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Phase 2a > Respiratory > Flashcards

Respiratory Flashcards

1
Q

Most common infective cause of COPD exacerbation?

A

Haemophilus influenzae

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2
Q

What are some infective causes of COPD exacerbation?

A
  • haemophilus influenzae
  • streptococcus pneumoniae
  • moraxella catarrhalis
  • haemophilus parainfluenzae
  • pseudomonas aeruginosa
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3
Q

Signs of a life-threatening asthma attack?

A
  • SpO2 < 92%
  • PEFR < 33%
  • silent chest
  • poor respiratory effort
  • altered consciousness
  • confusion / agitation
  • exhaustion
  • cyanosis
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4
Q

What are some side effects of salbutamol?

A
  • arrhythmias
  • headache
  • palpitations
  • tremor
  • hyperglycaemia
  • hypokalaemia (with high doses)
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5
Q

Most common lung cancer in non-smokers?

A

Adenocarcinoma

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6
Q

What is the CURB65 score?

A
  • Confusion
  • Urea > 7 mmol/L
  • Respiratory rate > 30
  • Blood pressure (systolic < 90 or diastolic < 60)
  • age > 65
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7
Q

What is the dyspnoea scale used for COPD?

A

Medical Research Council dyspnoea scale.

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8
Q

Grade 1 MRC dyspnoea scale?

A

Not troubled by breathlessness except on vigorous exertion.

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9
Q

Grade 2 MRC dyspnoea scale?

A

Short of breath when hurrying / walking up inclines.

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10
Q

Grade 3 MRC dyspnoea scale?

A

Walks slower than contemporaries because of breathlessness, or has to stop for breath when walking at own pace.

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11
Q

Grade 4 MRC dyspnoea scale?

A

Stops for breath after walking about 100m or stops after a few minutes’ walking on level ground.

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12
Q

Grade 5 MRC dyspnoea scale?

A

Too breathless to leave the house / breathless on dressing or undressing.

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13
Q

Second line COPD medication?

A

LABA

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14
Q

What is COPD?

A

Progressive obstructive airway disease that is not fully reversible. Results from disease of the airways and lung parenchyma (chronic bronchitis and emphysema).

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15
Q

What is meant by emphysema?

A

Damage to alveoli resulting in the rupture of alveolar walls. This creates large airspaces instead of many small ones.

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16
Q

Causes of COPD?

A
  • smoking
  • occupational exposures (coal dust)
  • alpha 1 antitrypsin deficiency
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17
Q

Risk factors for COPD?

A
  • smoking
  • older age
  • occupational exposure to dust, chemicals, etc
  • alpha 1 antitrypsin deficiency
  • air pollution exposure
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18
Q

Pathophysiology of chronic bronchitis?

A
  • chronic inflammation and fibrosis of the bronchi and bronchioles
  • neutrophil, T lymphocyte, and macrophage infiltration
  • leads to goblet cell hyperplasia, mucus hypersecretion, narrowing of small airways
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19
Q

Pathophysiology of emphysema?

A
  • inflammatory cells such as macrophages and neutrophils produce proteases (e.g. elastase)
  • elastase destroys elastin (important for the structural integrity of the alveoli)
  • alveoli become prone to collapse, and there is alveolar dilatation (may join neighbouring alveoli to form bullae)
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20
Q

How does COPD lead to cor pulmonale?

A
  • chronic hypoxia causes pulmonary artery vasoconstriction

- chronic elevation of pulmonary arterial pressure results in right heart failure

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21
Q

Signs and symptoms of COPD?

A
  • chronic productive cough
  • dyspnoea
  • sputum production
  • wheeze
  • pursed lip breathing
  • barrel chest
  • coarse crackles on auscultation
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22
Q

Why do COPD patients show pursed lip breathing?

A

Attempt to prevent alveolar collapse by increasing end expiratory pressure.

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23
Q

Signs of acute COPD exacerbation?

A
  • worsening dyspnoea and cough
  • increased sputum production or a change in sputum colour
  • pyrexia
  • signs of CO2 retention - flapping tremor and asterixis
  • accessory muscle use
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24
Q

What are signs of CO2 retention?

A
  • asterixis
  • flapping tremor
  • confusion
  • headache
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25
Q

Investigations for COPD?

A
  • spirometry with reversibility testing
  • CXR
  • sputum culture
  • ECG / echocardiogram if cor pulmonale suspected
  • serum A1AT
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26
Q

What does spirometry show in COPD?

A
  • normal / reduced FVC
  • reduced FEV1
  • FEV1 / FVC less than 70%
    No / little reversibility.
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27
Q

Differentials for COPD?

A
  • asthma
  • congestive heart failure
  • bronchiectasis
  • lung cancer
  • tuberculosis
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28
Q

Non-pharmacological management of COPD?

A
  • smoking cessation
  • inhaler technique
  • influenza and pneumococcal vaccinations
  • pulmonary rehabilitation
  • long term oxygen therapy if appropriate
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29
Q

Pharmacological management of COPD?

A
  1. SABA (salbutamol) / SAMA (ipratropium)
  2. LABA and LAMA / ICS (if responsive)
  3. LABA, LAMA, ICS
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30
Q

Example of inhaled corticosteroid?

A
  • fluticasone

- beclomethasone

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31
Q

Medication for excessive sputum production?

A

Mucolytics (e.g. carbocisteine).

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32
Q

Surgical options for COPD?

A
  • bullectomy

- lung transplantation

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33
Q

Management of acute COPD exacerbation?

A
  • oxygen to 88-92% (Venturi mask for specific concentration)
  • salbutamol / ipratropium nebulisers
  • oral / IV corticosteroids
  • antibiotics
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34
Q

What antibiotics are used in acute COPD exacerbation?

A
  • doxycycline

- co-amoxiclav

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35
Q

When is IV aminophylline / theophylline indicated in COPD?

A

Severe acute exacerbation - not first line.

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36
Q

What is asthma?

A

Chronic inflammatory condition of the airways, causing episodic exacerbations of bronchoconstriction.

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37
Q

What type of hypersensitivity reaction is allergic asthma?

A

Type 1 (IgE mediated).

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38
Q

What type of respiratory failure occurs in COPD?

A

Type 2 (low oxygen, high CO2).

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39
Q

What is meant by brittle asthma?

A

Asthma that worsens suddenly or severely, characterised by wide variation of PEFR despite high doses of steroids.

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40
Q

What are the two types of asthma?

A
  • eosinophilic (allergic)

- non-eosinophilic

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41
Q

What is atopy?

A

Genetic predisposition to allergic asthma, atopic dermatitis, allergic rhinitis.

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42
Q

What is Samter’s triad?

A

Aspirin-exacerbated respiratory disease:

  • asthma
  • aspirin sensitivity
  • nasal polyps
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43
Q

Risk factors for asthma?

A
  • smoking / smoking exposure
  • premature birth and low birth weight
  • family Hx of atopy
  • occupational exposure (dust, flour)
  • low socioeconomic status
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44
Q

Pathophysiology of asthma?

A
  • inhalation of allergens results in a type 1 hypersensitivity reaction in the airways
  • sensitisation results in the release of IgE antibodies from plasma cells, which bind to mast cell receptors
  • subsequent antigen exposure causes mast cell degranulation and histamine release, causing smooth muscle contraction, bronchoconstriciton, and inflammation
  • following the initial reaction, inflammatory cell recruitment occurs
  • fibrosis and airway remodelling eventually occur in response to chronic inflammation
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45
Q

Signs and symptoms of asthma?

A
  • dry cough
  • dyspnoea
  • expiratory wheeze
  • chest tightness
  • poor sleep / nocturnal symptoms
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46
Q

Provoking factors for an asthma attack?

A
  • allergens
  • infection
  • exercise
  • cold air
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47
Q

PEFR in life threatening asthma attack?

A

less than 33% of normal

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48
Q

Signs and symptoms of severe vs life threatening asthma attack?

A

Severe - can’t complete sentences due to worsening symptoms.

Life-threatening - silent chest, cyanosis, exhaustion, confusion, poor respiratory effort.

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49
Q

Investigations for asthma?

A
  • spirometry (with reversibility testing)
  • PEFR diary
  • immunoassay for allergen-specific IgE
  • CXR - normal or hyperinflated
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50
Q

Spirometry results in asthma?

A
  • FVC normal or reduced
  • FEV1 reduced
  • FEV1 / FVC less than 70%
    Asthma shows reversibility with bronchodilators.
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51
Q

Side effect of high doses of salbutamol?

A

Hypokalaemia

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52
Q

Acute management of severe asthma attack?

A
  • oxygen (target 94-98%)
  • salbutamol nebulisers
  • ipratropium nebulisers
  • IV hydrocortisone
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53
Q

Non-pharmacological management of asthma?

A
  • inhaler technique

- identify and avoid triggers

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54
Q

Pharmacological management of asthma?

A
  1. salbutamol (SABA)
  2. ICS (beclamethasone)
  3. LABA
  4. increase dose of ICS or leukotriene receptor antagonist
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55
Q

Example of leukotriene receptor antagonist?

A

Montelukast

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56
Q

Example of LABA?

A

Salmeterol

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57
Q

Side effects of ICS?

A
  • hoarse voice
  • sore throat
  • oral candidiasis
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58
Q

What is MART?

A

Maintenance and reliever therapy - combined corticosteroid and bronchodilator inhaler.

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59
Q

Common types of inhaler?

A
  • metered dose inhaler

- dry powder inhaler

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60
Q

Complications of asthma?

A
  • pneumonia
  • respiratory failure
  • pneumothorax
  • fatigue
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61
Q

What proportion of primary lung cancer is small cell lung cancer?

A

15-20%

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62
Q

What is small cell lung cancer?

A
  • high grade, neuroendocrine tumour

- associated with paraneoplastic syndromes

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63
Q

What are the three types of non-small cell lung cancer?

A
  • adenocarcinoma
  • squamous cell carcinoma
  • large cell lung cancer
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64
Q

Most common lung cancer?

A

Adenocarcinoma

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65
Q

Where in the lung does adenocarcinoma occur?

A

Peripheries

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66
Q

Where in the lung does squamous cell carcinoma occur?

A

Central parts

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67
Q

Characteristics of large cell lung cancer?

A
  • undifferentiated

- metastasises early

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68
Q

T1 lung cancer?

A

Tumour is less than 3cm and surrounded by the lung / visceral pleura. No involvement of the main bronchus.

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69
Q

T2 lung cancer?

A

Tumour is 3-5cm OR involves main bronchus (not carina) / invasion of visceral pleura.

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70
Q

T3 lung cancer?

A

Tumour is 5-7cm OR involves the chest wall, pericardium, phrenic nerve, or satellite nodules (accessory foci) in the same lobe.

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71
Q

T4 lung cancer?

A

Tumour > 7cm OR invades the mediastinum, diaphragm, heart, great vessels, carina / trachea, oesophagus OR separate tumour in different lobe of the same lung.

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72
Q

Which lung cancers is asbestos exposure associated with?

A
  • mesothelioma

- adenocarcinoma

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73
Q

Most common lung cancer in smokers?

A

Squamous cell

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74
Q

Most common lung cancer in non-smokers?

A

Adenocarcinoma

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75
Q

Clinical presentation of lung cancer?

A
  • cough
  • malaise
  • weight loss
  • haemoptysis
  • lymphadenopathy
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76
Q

Investigations for lung cancer?

A
  • CXR
  • CT thorax and abdomen
  • bronchoscopic biopsy
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77
Q

Management of lung cancer?

A
  • smoking cessation
  • surgical resection
  • radiotherapy
  • chemotherapy
  • palliative care
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78
Q

Common sites of lung cancer metastasis?

A
  • bones
  • brain
  • liver
  • adrenal glands
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79
Q

Paraneoplastic syndromes associated with small cell lung cancer?

A
  • hypercalcaemia
  • SIADH
  • Lambert-Eaton syndrome
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80
Q

What is mesothelioma?

A

Lung malignancy affecting the mesothelial cells of the pleura. Caused by asbestos inhalation.

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81
Q

What is a pulmonary embolism?

A

Occlusion / obstruction of the pulmonary artery or one of its branches.

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82
Q

What is meant by a non-massive PE?

A

Haemodynamically stable with no evidence of right heart strain.

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83
Q

What is meant by sub-massive PE?

A

Haemodynamically stable with evidence of right heart strain.

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84
Q

What is meant by massive PE?

A

Haemodynamic instability due to right heart strain / failure.

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85
Q

Typical cause of PE?

A

Embolus arising from DVT.

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86
Q

Pathophysiology of PE?

A
  • occlusion of one of the pulmonary arteries leads to absence of perfusion to that area of the lung
  • V/Q mismatch leads to hypoxia and breathlessness
  • V/Q mismatch may also cause elevated pulmonary arterial pressure, resulting in acute right heart failure
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87
Q

Why does infarction usually not occur in PE?

A

Prevented by the bronchial circulation.

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88
Q

Classic presentation of PE?

A

New onset shortness of breath, pleuritic chest pain, features of DVT.

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89
Q

Signs and symptoms of PE?

A
  • new onset shortness of breath
  • pleuritic chest pain
  • features of DVT
  • cough
  • haemoptysis
  • low grade fever
  • tachycardia
  • syncope / dizziness
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90
Q

Signs of right heart failure?

A
  • hypotension
  • raised JVP
  • tricuspid regurgitation (pan-systolic murmur)
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91
Q

Scoring system for PE?

A

Wells score:

  • greater than 4 means PE is likely
  • 4 or less means PE is unlikely
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92
Q

Gold standard investigation for PE?

A

CT pulmonary angiography

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93
Q

ECG changes in PE?

A
  • sinus tachycardia most common finding

- S1Q3T3 (acute right heart failure): deep S wave, Q wave, T wave inversion

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94
Q

What is the PESI score?

A

Pulmonary embolism severity index - predicts 30 day outcome of patients with confirmed PE.

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95
Q

Investigations to assess right heart strain in PE?

A
  • troponin
  • ECG
  • echocardiography
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96
Q

Empirical anticoagulation for suspected PE?

A

LMWH

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97
Q

First line anticoagulation for confirmed PE?

A

apixaban / rivaroxaban

98
Q

Second line anticoagulation for confirmed PE?

99
Q

When would you use thrombolysis for PE?

A

First line for massive PE.

100
Q

Long term management of PE?

A

Continue anticoagulation for 3 months.

101
Q

What is meant by latent TB?

A

TB infection is suppressed, there is no active disease.

102
Q

Cause of TB?

A

Mycobacterium complex:

  • mycobacterium tuberculosis
  • mycobacterium bovis
103
Q

Characteristics of mycobacterium tuberculosis?

A
  • aerobic
  • acid-fast
  • slow-growing
104
Q

How is TB spread?

A

Aerosolised droplets

105
Q

Risk factors for TB?

A
  • travel to an endemic country

- immunosuppression

106
Q

Pathophysiology of TB?

A
  • alveolar macrophages engulf the bacilli, but they survive and multiply within the macrophages
  • subsequent macrophage death and lysis releases the bacilli
  • immune response results in clearance, suppression, or progression to primary disease if inadequate
  • Th1 cells form caseating granulomas with macrophages, to contain the bacilli (latent TB)
107
Q

Why might latent TB become reactivated?

A
  • immunodeficiency (HIV)

- immunosuppressive drugs (infliximab)

108
Q

What is the Ghon focus?

A

Primary TB lesion - caseating granuloma.

109
Q

What is the Ghon complex?

A

Ghon focus with ipsilateral mediastinal lymph node involvement.

110
Q

What is a Ranke complex?

A

Calcified Ghon complex.

111
Q

Signs and symptoms of pulmonary TB?

A
  • cough
  • fever
  • weight loss
  • malaise
  • dyspnoea
  • haemoptysis
112
Q

What is miliary TB?

A

Disseminated haematogenous spread, leading to multiple organ failure.

113
Q

Options for TB screening?

A
  • mantoux test

- interferon gamma release assay

114
Q

What is the Mantoux test?

A
  • intradermal injection of tuberculin
  • type IV hypersensitivity reaction indicates latent TB
  • results affected by the BCG vaccine
115
Q

What is the interferon gamma release assay?

A

Tests for T-cell interferon game response to mycobacterium tuberculosis antigen. Unaffected by previous BCG vaccine.

116
Q

Investigations for TB?

A
  • sputum samples x3 for microscopy and culture

- CXR

117
Q

CXR findings in TB?

A
  • consolidation
  • cavitation (usually upper lobe)
  • effusion
118
Q

What type of vaccine is the BCG vaccine?

A

Live attenuated vaccine.

119
Q

Management of TB

A
  • isoniazid
  • rifampicin
  • pyrazinamide
  • ethambutol
120
Q

How does isoniazid work?

A

Inhibits mycolic acid synthesis - cell wall component of M. tuberculosis.

121
Q

Side effects of isoniazid?

A
  • polyneuropathy

- hepatotoxicity

122
Q

How does rifampicin work?

A

Inhibits RNA polymerase.

123
Q

Side effects of rifampicin?

A
  • red / orange staining of secretions

- hepatotoxicity

124
Q

Side effects of pyrazinamide?

A
  • hepatotoxicity

- gout

125
Q

How does ethambutol work?

A

Inhibits an enzyme needed for cell wall synthesis.

126
Q

Side effects of ethambutol?

A

Optic neuritis

127
Q

What is pneumonia?

A

Infection of the lung parenchyma, causing inflammation.

128
Q

What is hospital-acquired pneumonia?

A

Pneumonia presenting > 48 hours after hospital admission (not incubating at the time of admission).

129
Q

Causes of typical CAP?

A
  • streptococcus pneumoniae
  • moraxella catarrhalis
  • haemophilus influenzae
130
Q

Non-zoonotic causes of atypical CAP?

A
  • legionella pneumophila
  • mycoplasma pneumoniae
  • chlamydophila pneumoniae
131
Q

Zoonotic causes of atypical CAP?

A
  • coxiella burnetii

- chlamydia psittaci

132
Q

Causes of HAP?

A
  • staph aureus

- pseudomonas aeruginosa

133
Q

Fungal pathogens causing pneumonia?

A

Seen in immunocompromised patients:

  • aspergillus fumigatus
  • pneumocystis jirovecii
134
Q

Risk factors for pneumonia?

A
  • age > 65
  • residence in healthcare setting
  • COPD
  • immunocompromised
  • intubation and ventilation
135
Q

Signs and symptoms of pneumonia?

A
  • cough
  • dyspnoea
  • fever
  • purulent sputum
  • pleuritic pain
  • confusion
  • dull percussion
  • coarse crepitations
136
Q

SIADH indicates what cause of pneumonia?

A

Legionella pneumophila

137
Q

What is the CURB65 score?

A
  • confusion
  • urea > 7
  • respiratory rate >30
  • BP < 90 systolic or < 60 diastolic
  • over 65
138
Q

Management setting according to CURB65 score?

A

0-1 : outpatient
2: inpatient
3-5: HDU / ICU

139
Q

Complications of pneumonia?

A
  • parapneumonic effusion
  • pneumothorax
  • abscess
  • empyema
  • sepsis
140
Q

Investigations for pneumonia?

A
  • sputum cultures
  • blood cultures
  • CXR (consolidation, parapneumonic effusion, etc)
141
Q

Summary of pneumonia management?

A
  • oxygen titrated to saturations
  • IV / oral fluids
  • analgesia
  • antibiotics
142
Q

Antibiotics for mild CAP?

A

oral amoxicillin or doxycycline (if allergic)

143
Q

Antibiotics for severe CAP?

A

IV co-amoxiclav + clarithromycin

144
Q

Antibiotics for mild HAP?

A

Oral co-amoxiclav

145
Q

Antibiotics for severe HAP?

A

IV piperacillin / tazobactam

146
Q

Antibiotics for atypical pneumonia?

A

Does not respond to penicillins.

Clarithromycin / doxycycline.

147
Q

Treatment for fungal pneumonia?

A

Co-trimoxazole (trimethoprim and sulfamethoxazole).

148
Q

What is idiopathic pulmonary fibrosis?

A

Chronic condition characterised by progressive lung fibrosis of unknown aetiology.

149
Q

Signs and symptoms of idiopathic pulmonary fibrosis?

A
  • exertional dyspnoea
  • dry cough
  • fatigue
  • bilateral inspiratory crackles
  • clubbing
150
Q

Investigations for idiopathic pulmonary fibrosis?

A
  • spirometry
  • DLCO (diffusing capacity for carbon monoxide)
  • CXR
  • high-resolution CT
  • transbronchial biopsy
151
Q

Spirometry results in idiopathic pulmonary fibrosis?

A

Restrictive pattern:

  • reduced FEV1
  • reduced FVC
  • normal FEV1 / FVC ratio
152
Q

CT findings in idiopathic pulmonary fibrosis?

A
  • honeycombing

- traction bronchiectasis

153
Q

Management of idiopathic pulmonary fibrosis?

A
  • smoking cessation
  • pulmonary rehabilitation
  • oxygen therapy
  • biological therapies
  • lung transplant
154
Q

What biological therapies can be used for idiopathic pulmonary fibrosis?

A

Pirfenidone - anti-inflammatory and anti-fibrotic.

Nintedanib - acts on growth factor receptors (VEGF) implicated in IPF pathogenesis.

155
Q

What is sarcoidosis?

A

Multi-system granulomatous disorder, most commonly affecting the lungs.

156
Q

Typical sarcoidosis patient?

A

Black female aged 20-40 with progressive breathlessness, lymphadenopathy, and fatigue.

157
Q

Pathophysiology of sarcoidosis?

A

Non-caseating granulomas form - aggregations of macrophages with multi-nucleated giant cells in the centre, and scattered CD4 T lymphocytes.
Advanced pulmonary sarcoidosis leads to fibrosis.

158
Q

Systemic / pulmonary manifestations of sarcoidosis?

A
  • fatigue
  • lymphadenopathy
  • progressive breathlessness
  • wheezing
  • inspiratory creptitations
  • clubbing
159
Q

Extra-pulmonary manifestations of sarcoidosis?

A
  • liver nodules & cirrhosis
  • eye involvement (uveitis)
  • erythema nodosum / papular sarcoidosis
  • cardiomyopathy
  • renal disease
160
Q

What is Lofgren’s syndrome?

A

Acute variant of sarcoidosis:

  • bilateral hilar lymphadenopathy
  • erythema nodosum
  • arthralgia
  • fever
161
Q

Skin manifestations of sarcoidosis?

A
  • erythema nodosum
  • papular sarcoidosis
  • lupus pernio (nodular purple rash over nose and cheeks)
162
Q

Investigations for sarcoidosis?

A
  • spirometry
  • serum ACE (elevated)
  • CXR (lymphadenopathy)
  • high-resolution CT
  • transbronchial biopsy / bronchoalveolar lavage
  • ECG / echocardiography for cardiac involvement
163
Q

Spirometry results in sarcoidosis?

A

Restrictive pattern:

  • reduced FEV1
  • reduced FVC
  • normal FEV1 / FVC ratio
164
Q

Differentials for sarcoidosis?

A
  • tuberculosis
  • lymphoma
  • hypersensitivity pneumonitis
165
Q

Management of sarcoidosis?

A
  • steroids with bone protection
  • methotrexate / azathioprine
  • anti-TNF agents (infliximab)
  • lung transplant
166
Q

Prognosis for sarcoidosis?

A

Many patients experience spontaneous resolution within 6 months.

167
Q

What is bronchiectasis?

A

Obstructive lung disease characterised by irreversible abnormal dilatation of the airways. Often due to recurrent / severe infections.

168
Q

Infections that can lead to bronchiectasis?

A
  • mycobacterium tuberculosis
  • pseudomonas aeruginosa
  • streptococcus pneumoniae
  • haemophilus influenzae
  • aspergillus fumigatus
169
Q

Causes of bronchiectasis?

A
  • post-infectious
  • genetic disorder (CF, A1AT deficiency, primary ciliary dyskinesia)
  • COPD & asthma
  • connective tissue disorders
  • idiopathic
170
Q

Pathophysiology of bronchiectasis?

A
  • micro-organisms colonising the airways leads to chronic inflammation
  • this results in bronchial wall oedema and increased mucus production
  • recruitment of inflammatory cells and cytokine release leads to progressive airway destruction and dilatation
171
Q

Vicious cycle of bronchiectasis?

A

Bronchial damage makes patients more susceptible to subsequent airway colonisation.

172
Q

Signs and symptoms of bronchiectasis?

A
  • persistent sputum production
  • persistent cough
  • dyspnoea
  • fever
  • fatigue
  • lung crepitations
  • clubbing
  • wheeze
173
Q

Investigations for bronchiectasis?

A
  • blood cultures
  • sputum cultures
  • genetic testing (e.g. CFTR mutation, SERPINA1 mutation)
  • thin section CT (signet ring sign)
  • spirometry (obstructive pattern)
174
Q

What is the signet ring sign?

A

Sign of bronciectasis on thin section CT.

Cross section of dilated bronchus with its accompanying pulmonary artery branch.

175
Q

Management of bronchiectasis?

A
  • annual flu vaccine
  • physiotherapy for airway clearance
  • mucolytics (oral carbocisteine)
  • prophylactic antibiotics / antibiotics for acute exacerbation
  • bronchodilators
  • lung transplant
176
Q

What is cystic fibrosis?

A

Autosomal recessive multisystem disease caused by mutations in the CFTR gene.

177
Q

Aetiology of CF?

A

Mutations in CFTR gene on chromosome 7.

178
Q

Pathophysiology of CF?

A
  • mutations in the CFTR gene result in misfolded CFTR channel
  • this leads to impaired chloride ion transport, resulting in the production of thick mucus
179
Q

Most commonly identified CFTR mutation?

A

Delta-F508

180
Q

Common colonising organisms in children with CF?

A
  • staph aureus

- haemophilus influenzae

181
Q

Common colonising organisms in adults with CF?

A

pseudomonas aeruginosa

182
Q

Why does CF cause lung disease?

A
  • production of thick sticky mucus results in reduced clearance and airway obstruction
  • increases susceptibility to infection
  • leads to chronic bronchial damage and bronchiectasis
183
Q

Why does CF cause GI disease?

A
  • thick secretions impair biliary and pancreatic drainage

- pancreatic islets may also be damaged (diabetes mellitus)

184
Q

Clinical presentation of CF in neonates?

A
  • failure to pass meconium
  • failure to thrive
  • wet-sounding cough
185
Q

Signs and symptoms of CF?

A
  • wet-sounding cough
  • steatorrhoea
  • malabsorption
  • recurrent lower respiratory tract infections
  • clubbing
  • nasal polyps
186
Q

What is the screening test for CF?

A

Immuno-reactive trypsin test (newborn heel prick test). Positive result indicates CF as IRT is produced due to CF-related pancreatic damage.

187
Q

Investigations for CF?

A
  • pilocarpine-induced sweat test (chloride > 60 mmol/L)

- genetic testing

188
Q

Management of CF?

A
  • vaccinations
  • airway clearance techniques
  • pancreatic enzyme replacement
  • nebulised DNase (mucoactive agent)
  • antibiotics
  • oxygen therapy
  • lung transplant
  • CFTR modulators
189
Q

What are CFTR modulators?

A
  • tezacaftor and elexacaftor - increase amount of CFTR delivered to the cell surface
  • ivacaftor - facilitates CFTR channel opening
190
Q

Complications of CF?

A
  • recurrent pancreatitis
  • small bowel obstruction
  • pneumothorax
  • diabetes mellitus
  • cor pulmonale
191
Q

Why does pseudomonas colonisation increase morbidity and mortality in CF patients?

A
  • bacteria can form biofilms

- often become resistant to multiple antibiotics

192
Q

What is a pleural effusion?

A

Abnormal collection of fluid in the pleural space.

193
Q

What is a transudate?

A

Fluid has minimal protein content.

194
Q

What causes transudative pleural effusion?

A

Ultrafiltration due to changes in hydrostatic / oncotic pressure.

  • heart failure
  • hypoalbuminaemia
  • cirrhosis
  • nephrotic syndrome
195
Q

What is an exudate?

A

Fluid has high protein content.

196
Q

What causes exudative pleural effusion?

A

Inflammatory conditions affecting vessel permeability or lymphatic drainage.

  • infection (parapneumonic effusion, TB)
  • malignancy (breast / lung)
197
Q

Signs and symptoms of pleural effusion?

A
  • breathlessness
  • non-productive cough
  • pleuritic chest pain
  • reduced chest expansion
  • reduced breath sounds
  • stony dull percussion
198
Q

Investigations for pleural effusion?

A
  • pleural paracentesis
  • CXR
  • ultrasound
199
Q

Gold standard investigation for pleural effusion?

A

Pleural paracentesis - greater than 30g/L is an exudate.

200
Q

Management of pleural effusion?

A
  • address underlying cause
  • therapeutic paracentesis / chest drain
  • antibiotics (parapneumonic / empyema)
  • pleurodesis
201
Q

What is pleurodesis?

A

Procedure to induce pleural inflammation and fibrosis with a chemical sclerosant or manual abrasion.
Indicated if effusion if malignant / recurrent.

202
Q

What is a pneumothorax?

A

Collection of air in the pleural space.

203
Q

What is a tension pneumothorax?

A

One way valve system allows air into the inter-pleural space but does not let it escape. Results in increasing pressure, impaired venous return to the heart, and compromised cardiac output.

204
Q

Causes of pneumothorax?

A
  • trauma
  • primary spontaneous
  • secondary spontaneous (COPD, asthma)
205
Q

Cause of spontaneous pneumothorax?

A

Ruptured apical bleb / bullae.

206
Q

Clinical presentation of pneumothorax?

A

Sudden onset of (typically unilateral) pleuritic chest pain and dyspnoea.

207
Q

Signs of pneumothorax?

A
  • tracheal deviation
  • reduced chest expansion
  • reduced breath sounds
  • hyper-resonant percussion
208
Q

How does tension pneumothorax present?

A

Severe respiratory distress / haemodynamic instability.

209
Q

First line investigation for pneumothorax?

A
  • erect CXR

- CT / ultrasound if patient unable to sit upright

210
Q

What is considered a large pneumothorax?

A

> 2cm between chest wall and lung margin (at level of the hilum)

211
Q

Gold standard investigation for pneumothorax?

212
Q

Management of tension pneumothorax?

A
  • urgent decompression - large bore cannula in the 2nd intercostal space at the mid-clavicular line
  • place chest drain
  • high flow O2
213
Q

Management of large / symptomatic spontaneous pneumothorax?

A
  • needle aspiration (14-16G)

- small bore Seldinger chest drain (< 14F) if secondary or needle aspiration ineffective

214
Q

Management of small, asymptomatic spontaneous pneumothorax?

A

Observation and outpatient follow-up.

215
Q

Indications for pleurodesis for a pneumothorax?

A
  • pilot
  • bilateral pneumothoraces
  • persistent pneumothorax
216
Q

What is pulmonary hypertension?

A

Increased pressure in pulmonary arteries leading to right sided heart strain and systemic venous congestion.

217
Q

Causes of pulmonary hypertension?

A
  • left heart failure
  • pulmonary embolism
  • COPD
  • sarcoidosis
218
Q

Signs and symptoms of pulmonary hypertension?

A
  • dyspnoea
  • syncope
  • tachycardia
  • raised JVP
  • hepatomegaly
  • peripheral oedema
219
Q

Investigations for pulmonary hypertension?

A
  • ECG
  • CXR (dilated pulmonary arteries and RVH)
  • NT-proBNP
  • echocardiogram - measure pulmonary artery pressure
220
Q

Management of pulmonary hypertension?

A
  • IV prostanoids
  • endothelin receptor antagonists
  • phosphodiesterase-5 inhibitors (sildenafil)
    If secondary, manage the underlying cause.
221
Q

Complications of pulmonary hypertension?

A
  • right heart failure

- respiratory failure

222
Q

What is hypersensitivity pneumonitis?

A

Type III hypersensitivity reaction to an environmental allergen, resulting in parenchymal inflammation and destruction.

223
Q

What is a type III hypersensitivity reaction?

A

Mediated by the formation of antigen-antibody complexes.

224
Q

Another name for hypersensitivity pneumonitis?

A

Extrinsic allergic alveolitis.

225
Q

Causes of hypersensitivity pneumonitis?

A
  • bird-fanciers lung (bird droppings)
  • farmers lung (mouldy spores in hay)
  • mushroom workers lung
  • malt workers lung (mould on barley)
226
Q

Investigations for hypersensitivity pneumonitis?

A

Bronchoscopy and bronchoalveolar lavage - raised lymphocytes and mast cells.

227
Q

What is bronchoalveolar lavage?

A

Saline solution is put through a bronchoscope to wash the airways and capture a fluid sample.

228
Q

Management of hypersensitivity pneumonitis?

A
  • remove allergen

- steroids

229
Q

Types of pneumoconiosis?

A
  • silicosis
  • coal worker’s pneumoconiosis
  • chronic beryllium disease
  • asbestosis
230
Q

Investigations for pneumoconiosis?

A
  • CXR
  • spirometry
  • bronchoscopy biopsy / bronchoalveolar lavage
231
Q

Management of pneumoconiosis?

A
  • oxygen therapy
  • pulmonary rehabilitation
  • bronchodilator therapy
232
Q

What is granulomatosis with polyangiitis?

A

Small vessel vasculitis that can present with rapidly progressive glomerulonephritis and other systemic manifestations.
Previously called Wegener’s granulomatosis.

233
Q

Antibodies in granulomatosis with polyangiitis?

234
Q

Signs and symptoms of granulomatosis with polyangiitis?

A
  • dyspnoea, wheezing
  • haemoptysis
  • pleuritic chest pain
  • nasal discharge (may be bloody)
  • rhinosinusitis / otitis media
  • nephritic syndrome
  • fever, lethargy, weight loss, anorexia
  • pupuric rash
  • ophthalmic involvement
235
Q

Investigations for granulomatosis with polyangiitis?

A
  • biopsy of affected organs
  • serum anti-cANCA antibodies
  • urinalysis (haematuria and proteinuria)
  • CXR (infiltrates, consolidation, effusions)
236
Q

Management of granulomatosis with polyangiitis?

A
  • induction therapy with corticosteroids and rituximab

- maintenance therapy with rituximab monotherapy

237
Q

Most common cause of upper RTI?

A

Rhinoviruses

238
Q

Complications of upper RTI?

A
  • lower RTI
  • otitis media
  • rhinosinusitis
239
Q

What is a pancoast tumour?

A

Invades apical chest wall, compresses intercostal nerves, brachial plexus, sympathetic chain. Leads to Horner’s syndrome.

240
Q

Where do lung metastases come from?

A
  • breast
  • prostate
  • bladder
  • colon

Phase 2a (10 decks)

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