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MBChB Year 3 > Week 8 - Respiratory > Flashcards

Week 8 - Respiratory Flashcards

1
Q

What are 7 reasons why we measure lung function?

A
  1. Evaluation of breathless patient
  2. Screening for COPD/ occupational lung disease
  3. Lung cancer- fitness for treatment
  4. Pre-operative assessment
  5. Disease progression & treatment response
  6. Monitoring drug treatment toxic to lungs
  7. Pulmonary complications of systemic disease
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2
Q

What 2 lung function tests can we measure at home?

A
  1. Peak flow

2. Oximetry

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3
Q

What 2 lung function tests can we measure at the GP surgery?

A
  1. Spirometry

2. Oximetry

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4
Q

What 7 lung function tests can we measure in a specialist lab?

A
  1. Spirometry
  2. Transfer factor
  3. Lung volumes
  4. Blood gases
  5. Bronchial provocation testing
  6. Respiratory muscle function
  7. Exercise testing
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5
Q

What is spirometry?

A

Forced expiratory manoeuvre from total lung capacity followed by a full inspiration (best of 3)

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6
Q

What are the 4 pitfalls to spirometry?

A
  1. Appropriately trained technician
  2. Effort & technique dependent
  3. Patient frailty
  4. Pain, patient too unwell
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7
Q

What are 5 lung functions that can be directly measured?

A
  1. VC (vital capacity)
  2. IC (inspiratory capacity)
  3. IRV (inspiratory reserve volume)
  4. VT (normal tidal breathing)
  5. ERV (expiratory reserve volume)
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8
Q

What are 3 lung functions that can be indirectly measured?

A
  1. RV (residual volume)
  2. TLC (total lung capacity)
  3. FRC (functional residual capacity)
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9
Q

What 4 things can a time/volume plot measure?

A
  1. PEFR (peak expiratory flow rate)
  2. FEV1
  3. FVC
  4. FEV1/ FVC ratio (normal >70%)
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10
Q

What is a “normal” % of FEV1?

A

85% predicted

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11
Q

What 5 things should you correct for in FEV1 reference ranges?

A
  1. Age
  2. Gender
  3. Race
  4. Height
  5. Atmospheric values
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12
Q

What is obstructive lung disease generally?

A

Asthma or COPD

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13
Q

What is the FEV1/FVC ratio for obstructive lung disease?

A

<70%

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14
Q

Describe how the severity of COPD is stratified by % predicted FEV1?

A
  • Mild >80%
  • Mod 50-80%,
  • Severe 30-50%,
  • Very severe <30%
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15
Q

Describe reversibility testing?

A
  • Nebulised or inhaled salbutamol given

- Spirometry before & 15 min after salbutamol

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16
Q

What reversibility testing result is suggestive to asthma?

A

15% AND 400ml reversibility in FEV1

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17
Q

What are 4 investigations for asthma?

A
  1. PEFR testing
  2. Bronchial provocation
  3. Spirometry before & after trial of inhaled/ oral corticosteroid
  4. Reversibility testing
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18
Q

Describe PEFR testing for asthma?

A
  • Look for diurnal variation & variation over time
  • Response to inhaled corticosteroid
  • Occupational asthma
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19
Q

Describe the lung test results for restrictive lung disease?

A
  • FEV1 AND FVC reduced

- FEV1/ FVC ratio >70%

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20
Q

What are 6 causes of restrictive spirometry?

A
  1. Interstitial lung disease (stiff lungs)
  2. Kyphoscoliosis/ chest wall abnormality
  3. Previous pneumonectomy
  4. Neuromuscular disease
  5. Obesity
  6. Poor effort/ technique
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21
Q

What are the 4 stages to interpreting spirometry?

A
  1. Look at FEV1/ FVC ratio (if <70%, obstruction)
  2. If obstructed, look at % predicted FEV1 (severity) & any reversibility (COPD vs asthma)
  3. If FEV1/ FEV ratio normal, look at % predicted FVC (if low, suggests restrictive abnormality)
  4. Can also get mixed picture (obesity & COPD)
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22
Q

Describe the transfer factor (TLCO, KCO, DLCO)?

A
  • Single breath of a very small concentration of carbon monoxide
  • CO has very high affinity to Hb
  • Measure concentration in expired gas to derive uptake in the lungs
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23
Q

What 4 things is transfer factor affected by?

A
  1. Alveolar surface area
  2. Pulmonary capillary blood volume
  3. Haemoglobin concentration
  4. Ventilation perfusion mismatch
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24
Q

What 4 things is transfer factor reduced in?

A
  1. Emphysema
  2. Interstitial lung disease
  3. Pulmonary vascular disease
  4. Anaemia (increased in polychthaemia)
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25
Q

What are you unable to measure by spirometry?

A

Residual volume

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26
Q

What are the 2 methods of measuring lung volumes?

A
  1. Helium dilution (inspire known quantity of inert gas)
  2. Body plethysmography (respiratory manoevures in a sealed box lead to changes in air pressure- can derive lung volumes. Archimedes principle!)
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27
Q

When is lung volumes reduced?

A

Restrictive lung disease

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28
Q

When is RV & RV/TLC increased?

A

Obstructive lung disease

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29
Q

What is oximetry?

A

Non-invasive measurement of saturation of haemoglobin by oxygen

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30
Q

What does oximetry depend on?

A
  • Oxyhaemoglobin & deoxyhaemoglobin absorbing infrared light differently
  • Adequate perfusion (shock, cardiac failure)
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31
Q

What does oximetry NOT measure?

A

Carbon dioxide (so not ventilation)

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32
Q

What is the main downfall of oximetry?

A

False reassurance in a patient on oxygen with normal saturations (acute asthma, COPD, hypoventilation)

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33
Q

What are the 4 main causes of hypoxaemia?

A
  1. Hypoventilation (eg drugs, neuromuscular disease)
  2. Ventilation/ perfusion mismatch (eg COPD, pneumonia)
  3. Shunt (eg congenital heart disease)
  4. Low inspired oxygen (altitude, flight)
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34
Q

Describe ventilation perfusion mismatch?

A
  • Happens to a degree in normal lungs
  • Main cause of hypoxaemia in medical patients
  • Areas of lung that are perfused but not well ventilated (eg pneumonic consolidation)
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35
Q

What causes hypoxaemia?

A

Mixing of blood from poorly ventilated & well ventilated parts of the lung

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36
Q

What doesn’t fully correct with oxygen administration?

A

Ventilation perfusion mismatch

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37
Q

What is an extreme form of V/Q mismatch?

A

Shunt

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38
Q

What is the pO2 & pCO2 of air?

A
  • pO2 = 21 kPa

- pCO2 = 0.03 kPa

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39
Q

What is the alveolar oxygen equation?

A

PAO2 = FiO2 – (1.25 x PaCO2)

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40
Q

What is PAO2?

A

Alveolar oxygen partial pressure, kPa

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41
Q

What is FiO2?

A

Inspired oxygen concentration, kPa

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42
Q

How can Arterial pO2 (PaO2) be measured?

A

Directly measured- ABG

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43
Q

What is the difference between calculated alveolar pO2 & the arterial pO2?

A

The alveolar arterial (A-a) oxygen gradient

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44
Q

What should the difference between alveolar & arterial oxygen partial pressure be?

A

<2-4 kPa (more than this suggests V/Q mismatch)

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45
Q

Describe the 3 steps to blood gas analysis from a respiratory perspective?

A
  • Always look at the pO2 first (Is the patient in respiratory failure requiring additional oxygen?)
  • Look at the PCO2 (type 1 vs type 2 respiratory failure)
  • Consider acid base balance
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46
Q

Describe the blood gas analysis of acute respiratory acidosis (acid base balance)?

A
  • Elevated pCO2
  • Normal bicarbonate
  • Acidosis
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47
Q

Describe the blood gas analysis of compensated respiratory acidosis?

A
  • Elevated pCO2
  • Elevated bicarbonate (renal compensation)
  • Not acidotic
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48
Q

Describe the blood gas analysis of acute on chronic respiratory acidosis?

A
  • Elevated pCO2
  • Elevated bicarbonate
  • Acidotic
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49
Q

Define Chronic Obstructive Pulmonary Disease (COPD)?

A

Characterised by airflow obstruction which is usually progressive, not fully reversible & does not change markedly over several months

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50
Q

What is COPD commonly caused by?

A

Smoking

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51
Q

Only 15-20% of smokers get COPD, so what are 4 other factors which can cause COPD?

A
  1. Environmental pollution
  2. Burning of biomass fuels
  3. Occupational dusts
  4. Alpha 1 anti-trypsin deficiency
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52
Q

List the 6 effects of cigarette smoking on the lungs?

A
  1. Cilial motility reduced
  2. Airway inflammation
  3. Mucus hypertrophy & hypertrophy of Goblet cells
  4. Increased protease activity, anti-proteases inhibited
  5. Oxidative stress
  6. Squamous metaplasia → higher risk of lung cancer
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53
Q

Describe alpha 1 antitrypsin deficiency (genetic risk of COPD)?

A
  • Present in 1-3 % of COPD patients
  • Serine proteinase inhibitor
  • M alleles normal variant
  • SS & ZZ homozygotes have clinical disease
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54
Q

Describe the 2 part clinical syndrome of COPD?

A
  1. Chronic Bronchitis- production of sputum on most days for at least 3 months in at least 2 years
  2. Emphysema- abnormal, permanent enlargement of the airspaces distal to the terminal bronchioles
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55
Q

Describe the morphology of chronic bronchitis?

A
  • Loss of interstitial support
  • Increased epithelial mucous cells
  • Mucus gland hyperplasia
  • Squamous metaplasia
  • Infiltration with neutrophils & CD8+ lymphocytes
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56
Q

What does the inflammation in chronic bronchitis lead to?

A

Scarring & thickening of airway (>4mm in diameter)

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57
Q

Describe small airways disease?

A
  • “Bronchiolitis” in airways of 2 -3 mm
  • May be an early feature of COPD
  • Narrowing of the bronchioles due to mucus plugging, inflammation & fibrosis
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58
Q

List the 3 cell types present in COPD inflammation?

A
  1. Macrophages
  2. CD8 & CD4 T
  3. Neutrophils
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59
Q

List the 4 types of inflammatory markers present in COPD inflammation?

A
  1. TNF, IL-8 & other chemokines
  2. Neutrophil elastase, proteinase 3, cathepsin G (from activated neutrophils)
  3. Elastase & MMPs (from macrophages)
  4. Reactive oxygen species
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60
Q

What persists after smoking ceased?

A

Airway inflammation

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61
Q

Describe Centri-acinar Emphysema?

A
  • Damage around respiratory bronchioles

- More in upper lobes

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62
Q

Describe Pan-acinar Emphysema?

A
  • Uniformly enlarged from the level of terminal bronchiole distally
  • Can get large bullae
  • Associated with α1 anti-trypsin deficiency
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63
Q

What does emphysema cause?

A

Consequent loss of surface area for gas exchange

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64
Q

List the 3 types of emphysema?

A
  1. Centriacinar
  2. Paraseptal
  3. Panacinar
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65
Q

List the 4 mechanism of airflow obstruction in COPD?

A
  1. Loss of elasticity & alveolar attachments due to emphysema –> airways collapse on expiration
  2. Goblet cell metaplasia with mucus plugging of lumen
  3. Inflammation of airway wall
  4. Thickening of bronchiolar wall
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66
Q

What does loss of elasticity and alveolar attachments due to emphysema cause?

A

Airway collapse on expiration → Airtrapping & hyperinflaltion → increased work of breathing → breathlessness

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67
Q

How do you diagnose COPD?

A

People who are over 35, & smokers or ex-smokers, with any of:

  • Exertional breathlessness
  • Chronic cough
  • Regular sputum production
  • Frequent winter ‘bronchitis’
  • Wheeze
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68
Q

What is the spirometry result for COPD (obstructive lung disease)?

A

FEV1/FVC ratio < 70 % (both reduced)

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69
Q

What are the 5 types of treatment for COPD?

A
  1. Inhaled bronchodilators
  2. Inhaled corticosteroids
  3. Oral theophyllines
  4. Mucolytics - carbocysteine
  5. Nebulised therapy
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70
Q

What are 2 examples of inhaled bronchodilators used for COPD?

A
  1. Short-acting: salbutamol

2. Long acting: salmeterol, tiotropium

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71
Q

What are 2 examples of inhaled corticosteroids used for COPD?

A
  1. Budesonide & fluticasone: combination inhalers

2. Oxygen therapy

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72
Q

What 2 types of treatment would you give for A type (low risk) COPD?

A
  1. SABA

2. SAMA

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73
Q

What 2 types of treatment would you give for B type (low risk) COPD?

A
  1. LABA or LAMA

2. LABA + LAMA

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74
Q

What 3 types of treatment would you give for C type (high risk) COPD?

A
  1. LAMA
  2. LABA + LAMA
  3. LABA + ICS
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75
Q

What combination of treatments would you give for D type (high risk) COPD?

A

LABA + LAMA + ICS + theophylline + macrolide

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76
Q

List 4 endotypes in the personalised treatment of COPD?

A
  1. Persistent systemic inflammation
  2. Eosinophilic or Th2 high COPD
  3. Persistent pathogenic bacterial colonisation
  4. α-1 antitrypsin deficiency
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77
Q

List 3 phenotypes in the personalised treatment of COPD?

A
  1. Frequent exacerbators
  2. Persistent breathlessness
  3. Chronic bronchitis
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78
Q

How is a decline in lung function measured?

A

Forced expiratory volume in 1 second (FEV1)

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79
Q

Describe the symptoms of FEV1 <80% predicted?

A

Worsening airflow limitation & shortness of breath typically developing on exertion

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80
Q

Describe the symptoms of FEV1 <50% predicted?

A

Increased breathlessness & repeated exacerbations impact patient quality of life & will likely lead to increased hospitalisation

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81
Q

Describe the symptoms of FEV1 <30% predicted?

A
  • Severe breathlessness & respiratory failure, marked by hypoxemia
  • Pulmonary hypertension usually develops following severe hypoxemia
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82
Q

What are 2 systemic, extra pulmonary effects of COPD (decreased FEV1)?

A
  1. Systemic inflammation

2. Skeletal muscle dysfunction

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83
Q

What is a blue bloater (respiratory failure in COPD)?

A
  • Low respiratory drive
  • Type 2 respiratory failure
  • ↓PaO2, ↑PaCO2
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84
Q

List the 7 signs of a blue bloater (respiratory failure in COPD)?

A
  1. Cyanosis
  2. Warm peripheries
  3. Bounding pulse
  4. Flapping tremor
  5. Confusion, drowsiness,
  6. Right heart failure
  7. Oedema, raised JVP
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85
Q

What is a pink puffer (respiratory failure in COPD)?

A
  • High respiratory drive
  • Type 1 respiratory failure
  • ↓PaO2, ↓PaCO2
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86
Q

List the 6 signs of a pink puffer (respiratory failure in COPD)?

A
  1. Desaturates on exercise
  2. Pursed lip breathing
  3. Use accessory muscles
  4. Wheeze
  5. Indrawing of intercostals
  6. Tachypnoea
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87
Q

What does ACOS stand for?

A

Asthma-COPD overlap syndrome

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88
Q

Describe the inflammatory processes involved in asthma?

A

Sensitising agent –> Asthmatic airway inflammation (CD4+, T lymphocytes, eosinophils) –> Completely reversible

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89
Q

Describe the inflammatory processes involved in COPD?

A

Noxious agent –> COPD airway inflammation (CD8+, T lymphocytes, macrophages, neutrophils) –> Irreversible

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90
Q

What is the likely cause if you have >400ml reversibility on spirometry?

A

Asthma

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91
Q

What is the only intervention which slows the progression of COPD?

A

Smoking cessation

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92
Q

List the 4 clinical features of COPD?

A
  1. Nearly all smokers or ex-smokers
  2. Rarely get symptoms under 35 years
  3. Chronic productive cough
  4. Persistent & progressive breathlessness
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93
Q

List the 5 clinical features of asthma?

A
  1. Possibly a smoker or ex-smoker
  2. Ofter have symptoms under 35 years
  3. Variable breathlessness
  4. Night time waking with breathlessness &/or wheeze
  5. Significant diurnal or day to day variability of symptoms
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94
Q

What is respiratory failure defined as?

A

PO2 <8 kPa at sea level

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95
Q

What SpO2 should you aim for in patients with exacerbated COPD?

A

88-92%

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96
Q

What is the normal SpO2 & PaO2 (kPa)?

A
  • SpO2= 95-99%

- PaO2= 10-13.3%

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97
Q

What is the mild hypoxaemia SpO2 & PaO2 (kPa)?

A
  • SpO2= 90-95%

- PaO2= 8-10%

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98
Q

What is the moderate hypoxaemia SpO2 & PaO2 (kPa)?

A
  • SpO2= 85-90%

- PaO2= 6.7-8%

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99
Q

What is the severe hypoxaemia SpO2 & PaO2 (kPa)?

A
  • SpO2= <85%

- PaO2= <6.7%

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100
Q

Describe the ABG results of metabolic acidosis?

A
  • Increased H+
  • Decreased HCO3 (primary derangement)
  • Decreased PCO2 (if compensation is present)
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101
Q

Describe the ABG results of metabolic alkalosis?

A
  • Decreased H+
  • Increased HCO3 (primary derangement)
  • Increased PCO2 (if compensation is present)
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102
Q

Describe the ABG results of respiratory acidosis?

A
  • Increased H+
  • Increased PCO2 (primary derangement)
  • Increased HCO3 (if compensation is present)
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103
Q

Describe the ABG results of respiratory alkalosis?

A
  • Decreased H+
  • Decreased PCO2 (primary derangement)
  • Decreased HCO3 (if compensation is present)
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104
Q

What is the normal range blood gas analysis of H+?

A

36-43 nmol/L

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105
Q

What is the normal range blood gas analysis of pH?

A

7.35 – 7.45

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106
Q

What is the normal range blood gas analysis of PCO2?

A

4.6 – 6.0 kPa

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107
Q

What is the normal range blood gas analysis of PO2?

A

10.5 – 13.5 kPa

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108
Q

What is the normal range blood gas analysis of actual bicarbonate (calculated)?

A

23 – 30 mmol/L

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109
Q

What is the Henderson-Hasselbalch equation?

A

pH = pK + log [HCO3- ] / alphaPCO2

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110
Q

According to the Henderson-Hasselbalch equation what 3 things have a fixed relationship?

A

[H+], P CO2 & [HCO3-]

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111
Q

What are the 4 questions to ask when assessing ABGs?

A
  1. Acidaemia or Alkalaemia?
  2. Primary disturbance: respiratory or metabolic?
  3. For a metabolic acidosis, is there a high anion gap?
  4. Is there compensation? Appropriate?
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112
Q

Describe acid/base compensation?

A
  • Usually partial
  • Respiratory compensations (to metabolic disorders) happen quickly (mins- hrs)
  • Metabolic compensations are slower (many hrs-days)
  • Greater compensation in chronic than acute disorders
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113
Q

Is over compensation possible?

A

NO- look for another abnormality

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114
Q

What are the 4 buffers for ABG compensation?

A
  1. Haemoglobin
  2. Plasma proteins
  3. Bicarbonate
  4. Phosphate
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115
Q

What are 2 reasons as to why we recognise compensation?

A
  1. Primary disorders with compensation vs mixed disorders

2. Mild disorders can get fully compensated, but should make you think of mixed disorders

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116
Q

Describe compensation?

A
  • Compensatory responses for metabolic disorders are not as predictable as respiratory disorders
  • The compensation is always in the same direction as the initial chemical change
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117
Q

What concurrent acid-base disturbance is impossible?

A

Concurrent respiratory alkalosis & respiratory acidosis

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118
Q

When should you suspect a mixed acid-base disorder?

A
  • Inadequate/too extreme compensation
  • The pCO2& HCO3 concentration become abnormal in the opposite direction (one is elevated while the other is reduced)
  • pH is normal but pCO2or HCO3 concentration is abnormal
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119
Q

What acid-base disturbance is shown in respiratory acidosis & metabolic acidosis?

A

pCO2high & the HCO3low

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120
Q

What acid-base disturbance is shown in respiratory alkalosis & metabolic alkalosis?

A

pCO2low & the HCO3high

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121
Q

For a patient with metabolic acidosis, what 3 other things would you like to measure?

A
  1. Lactate
  2. Ketones (urine dipstick/blood)
  3. Glucose (may be elevated in very ill patients due to stress response/dextrose given as IV fluids)
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122
Q

What is the anion gap equal to?

A

[Na+] – ([Cl-] + [HCO3-])

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123
Q

What is the normal anion gap?

A

8–16 mmol/L

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124
Q

What is the anion gap used in?

A

Differential diagnosis of metabolic acidosis

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125
Q

Give 4 examples of disorders causing a raised anion gap (excess production of H+/ inability to excrete it)?

A
  1. Renal failure
  2. Diabetic or other ketoacidosis
  3. Lactic acidosis
  4. Toxins e.g. salicylate, some IEM
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126
Q

Give 4 examples of disorders causing a normal anion gap (Excess HCO3- loss)?

A
  1. Renal tubular acidosis
  2. Diarrhoea
  3. Carbonic anhydrase inhibitors
  4. Ureteric diversion
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127
Q

What is the serum osmolal gap equal to?

A

Measured osmolality – calculated osmolality

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128
Q

What is the calculated osmolality equal to?

A

2X (Na+ + K+) + urea + glucose (all in mmol/L)

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129
Q

What is the normal osmolal gap?

A

<10mOsm/kg

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130
Q

What can also influence the osmolal gap?

A

Ethanol

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131
Q

What does non-invasive ventilation in COPD provide?

A

Positive pressure to the airways to support breathing

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132
Q

When would you consider non-invasive ventilation in COPD?

A

Respiratory acidosis (pH < 7.35, H+ > 45) present or if acidosis persists despite maximal medical therapy

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133
Q

What 5 clinical features of COPD does non-invasive ventilation reduce?

A
  1. Respiratory rate
  2. Improves dyspnoea & gas exchange
  3. Mortality
  4. Need for ventilation in ITU
  5. Length of hospital stay
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134
Q

What is cor pulmonate a clinical syndrome of?

A
  1. Right heart failure secondary to lung disease

2. Salt & water retention leading to peripheral oedema

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135
Q

What are the 4 signs of cor pulmonale?

A
  1. Peripheral oedema
  2. Raised jugular venous pressure
  3. A systolic parasternal heave
  4. Loud pulmonary second heart sound
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136
Q

What 2 things may develop in cor pulmonale?

A
  1. Pulmonary hypertension

2. Right ventricular hypertrophy may develop

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137
Q

What is the treatment for cor pulmonale?

A

Diuretics to control peripheral oedema

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138
Q

What 2 things can severe COPD lead to?

A
  1. Chronic hypercapnic respiratory failure with serum biochemical compensation
  2. Cor pulmonale
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139
Q

Why is the lung vulnerable to allergy (pathology)?

A

Because its anatomically weak & has the same entry & exit portal

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140
Q

What are the 2 solutions to the unfortunate design of the lungs?

A
  1. Speed/flow airway calibre

2. Surface area

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141
Q

What is the definition of an allergy?

A

Immune system mediated intolerance

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142
Q

What are the 4 things that you need for an allergy?

A
  1. Trigger
  2. Recognition- specific response to the trigger
  3. Memory- enables you to remember the specific response
  4. Immunological response
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143
Q

Describe the immediate allergic response?

A
  • Recognition of the trigger by APC & T-cells
  • IL-4 & IL-33
  • Response via IgE, Mast cells
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144
Q

Describe the delayed allergic response?

A
  • Recognition of the trigger by APC & T-cell
  • IL-12 + IFN
  • Response via reactive T cells
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145
Q

What are the 3 types of clinical reactions to allergy?

A
  1. Acute
  2. Sudden/Slow
  3. Progressive
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146
Q

What does chronic allergy lead to?

A
  • Tissue remodelling

- Acute inflammation –> repair

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147
Q

Describe allergy in the airways?

A

Affects airflow:

  • Increases resistance
  • Causes wheeze/stridor (turbulence)
  • Measured by spirometry
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148
Q

What 2 tests are not helpful in allergy of the airways?

A
  1. Imaging (CXR)

2. Gas transfer

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149
Q

What are the upper/extra thoracic airways not susceptible to?

A

Intra-thoracic pressure

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150
Q

What is the trachea not susceptible to?

A

Intra-thoracic pressure

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151
Q

Describe extra-thoracic disease clinically?

A
  • Stridor
  • Flow-volume loops
  • CXR not helpful
  • Aspiration to Right middle/lower lobe
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152
Q

What is an example of extra-thoracic disease?

A

Laryngeal oedema (thyroid, scarring, epiglotitis)

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153
Q

What is bronchial disease susceptible to?

A

Intra-thoracic pressure

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154
Q

What are the clinical consequences of bronchial disease?

A
  • Medium-Small airways flaccid walls so not supported by cartilage
  • Expiratory phase narrowing: wheeze
  • Muco-ciliary clearance impairment (sputum)
  • Characteristic flow-volume loops
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155
Q

What is unhelpful in testing bronchial disease?

A

CXR – unhelpful (hyperinflation)

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156
Q

Describe the spirogram (flow-volume loops) for extrathoracic disease?

A
  • Box like

- Volume has decreased

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157
Q

Describe the spirogram (flow-volume loops) for intrathoracic disease?

A
  • Collapsed airway so can’t push air through

- Variable

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158
Q

Describe the physiological definition of asthma?

A

Reversible/variable airflow obstruction

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159
Q

Describe the pathological definition of asthma?

A

Airways inflammation/allergy

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160
Q

Describe the clinical definition of asthma?

A

Triggers- cold, exercise, cat, noctrunal/diurnal

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161
Q

Describe the morphological appearance of pathological asthma?

A
  • Inflammation
  • Scabby epithelium
  • Thickened BM
  • Thickened smooth muscle
  • Mast cells in smooth muscle
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162
Q

Describe the presentation of physiological asthma?

A
  • Yellow mucous
  • Repair pathways
  • Non elastic airways
  • Increased responsiveness
  • Increased sensitivity
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163
Q

Describe the presentation of clinical asthma?

A
  • Cough/wheeze
  • Hyper-reactivity
  • Hyper-sensitivity
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164
Q

What are the 3 points to a definition of clinical asthma?

A
  1. Appropriate symptoms with signs- Wheeze, cough, yellow/clear sputum, breathlessness, exercise intolerance
  2. Episodic, triggered, variable- paroxysmal
  3. Respond to asthma therapies
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165
Q

What is characteristic of asthmatic airways?

A

Airway smooth muscle hypertrophy with infiltration of mast cells

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166
Q

Broadly, what 3 things are needed for a diagnosis of asthma?

A
  1. Appropriate clinical story
  2. Supportive physiological tests
  3. Clinical signs at times of symptoms
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167
Q

What are asthmatic “twitchy airways” due to?

A

Bronchial hypersensitivity (they are more sensitive to histamine)

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168
Q

Describe the effect of salbutamol on an asthmatic patient?

A

Reversible airflow obstruction => 15% improvement in FEV1 after 5mg nebuliser salbutamol

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169
Q

Where would you perform a bronchial challenge when testing an asthmatic patient?

A

Plethysmography Box

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170
Q

What 4 cells are involve in airway allergies (asthmatics)?

A
  1. Mast cells
  2. Lymphocytes
  3. Macrophages
  4. Epithelial cells
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171
Q

What 6 types of cytokine inflammatory cells are involved in airway allergies (asthmatics)?

A
  1. IL-5
  2. TSLP
  3. IL-13
  4. TNF alpha
  5. TGF beta
  6. VEGF
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172
Q

What does airway allergy drive?

A

Eosinophillic inflammation

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173
Q

Describe inflammatory airway allergy?

A
  • Corticosteroid responsive disease
  • Routinely identified in airways of asthma
  • If stimulated will drive an asthma phenotype
    (viral infections, late allergic reactions)
  • Multiple candidate genes & non-hierarchical genes associated with asthma are inflammatory
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174
Q

What drives allergic airways inflammation/remodelling?

A

Cytokines

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175
Q

In what 4 ways do cytokines in allergic airways cause airway remodelling?

A
  1. Angiogenesis
  2. Epithelial cell damage
  3. Fibrosis
  4. Smooth muscle hypertrophy
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176
Q

What are the 4 established specific treatments for asthma?

A
  1. Bronchodilators
  2. Anti-leukotriene receptor drugs
  3. Corticosteroids
  4. Anti-IgE biological therapy
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177
Q

What are 4 future specific treatments for asthma?

A
  1. Immunotherapy
  2. Biological therapies (TNF, IL-5, IL-13)
  3. Thermoplasty
  4. Nerve ablation
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178
Q

List 9 triggers of extrinsic allergic alveoli’s?

A
  1. Bird dander
  2. Mushroom worker’s lung
  3. Farmer’s lung (fungal spores)
  4. Aspergillus lung
  5. Cheese workers
  6. Wheat weevil
  7. Mollusc shell workers
  8. Malt worker’s lung
  9. Humidifier lung
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179
Q

Describe the acute illness which can occur in allergic disease in the lung parenchyma?

A
  • 4-6 hours after exposure
  • Wheeze, cough, fever, chills, headache, myalgia, malaise, fatigue
  • May last several days
  • Serum sickness illness
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180
Q

What are 3 factors of immune complex disease?

A
  1. Acute inflammation
  2. Neutrophils
  3. Consolidation
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181
Q

What is the pathological consequence of Peripheral/Parenchymal disease?

A

Thickening of the septae, filling of the alveolus with fluid

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182
Q

List the 2 clinical consequences of Peripheral/Parenchymal disease?

A
  1. Loss of O2- Hypoxaemia (normal CO2)

2. Air space shadowing on CXR

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183
Q

What 2 things occur with chronic exposure to Peripheral/Parenchymal disease?

A
  1. Fibrosis- Interstitial scarring from chronic tissue remodelling/repair pathways
  2. Emphysema- Interstitial destruction from neutrophillic enzyme release
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184
Q

What law is regarding passive diffusion?

A

Fick’s law

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185
Q

What law is regarding solubility?

A

Henry’s Law

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186
Q

How is solubility affected in Peripheral/Parenchymal disease?

A
  • Emphysema= reduced surface area

- Pulmonary fibrosis= increased distance

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187
Q

What are the 3 clinical consequences of Peripheral/Parenchymal disease?

A
  • Reduced oxygen transport into the blood stream
  • Measured by carbon monoxide gas transfer during full PFTs
  • Airspace shadowing on CXR
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188
Q

Describe extrinsic allergic alveolitis and the 2 types of hypersensitivities associated?

A
  • Serum sickness or immune complex disease
  • Sub acute days to weeks
  • Type IV T-cell mediated reaction
  • Type III hypersensitivity reaction (antigen-antibody complexes)
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189
Q

What does chronic extrinsic allergic alveolitis lead to?

A

Fibrosis & emphysema

- Final pathway of all chronic inflammatory conditions

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190
Q

What are 3 ways to manage extrinsic allergic alveolitis?

A
  1. Allergy- avoid trigger (occupation)
  2. Inflammation- corticosteroids (neutrophils are modestly steroid responsive, cytotoxics)
  3. Oxygen supplementation
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191
Q

What is the definition of obstructive sleep apnoea?

A

Recurrent episodes of partial or complete upper (pharyngeal) airway obstruction during sleep, intermittent hypoxia & sleep fragmentation

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192
Q

How does obstructive sleep apnoea syndrome manifest clinically?

A

Excessive daytime sleepiness

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193
Q

Describe the mechanism of obstructive sleep apnoea?

A

Pharyngeal narrowing –> Negative thoracic pressure –> Arousal –> Sleep disruption / Blood pressure surge

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194
Q

What are 3 consequences of obstructive sleep apnoea causing sleep disruption?

A
  1. Sleepiness
  2. Reduced quality of life
  3. Road traffic accidents
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195
Q

What are 2 consequences of obstructive sleep apnoea due to blood pressure surge?

A
  1. Heart attacks

2. Strokes

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196
Q

What happens to the airways in obstructive sleep apnoea?

A

Airway collapses, stopping air from travelling to & from your lungs, disturbing your sleep

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197
Q

Describe the epidemiology of obstructive sleep apnoea?

A
  • 25,000,000 snorers in UK (40% population)
  • 5% of UK adults thought to have undiagnosed OSA
  • 250,000 men have severe OSA in UK
  • Men > Premenopausal females
  • Average age of presentation 40-50 years old
  • Incidence increasing with obesity epidemic
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198
Q

List the 6 symptoms of obstructive sleep apnoea?

A
  1. Snorer
  2. Witnessed apnoeas
  3. Disruptive sleep- nocturia/choking/dry mouth/ sweating
  4. Unrefreshed sleep
  5. Daytime somnolence
  6. Fatigue/ Low mood/ Poor concentration
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199
Q

What are the 7 specialties that patients with obstructive sleep apnoea can be referred on to?

A
  1. GP
  2. ENT
  3. Pre-operative assessment for elective surgery
  4. Post-operative presentation
  5. Weight management clinics
  6. Diabetes clinic
  7. Neurology
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200
Q

What is important in a history of obstructive sleep apnoea?

A

History from partner

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201
Q

List 7 things you should assess in a clinical examination of obstructive sleep apnoea?

A
  1. Weight
  2. BMI
  3. BP
  4. Neck circumference (>40cm)
  5. Craniofacial appearance (Retrognathia, Micrognathia)
  6. Tonsils
  7. Nasal patency
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202
Q

What are 3 questionnaire that can assess a patients excessive daytime sleepiness?

A
  1. The Epworth Sleepiness Score
  2. The STOP-BANG Questionnaire
  3. The Berlin Questionnaire
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203
Q

What are the 6 investigations in the limited Polysomnography (Limited Sleep Study)?

A
  1. 5 channel home study
  2. Oxygen Saturations
  3. Heart Rate
  4. Flow
  5. Thoracic and Abdominal effort
  6. Position
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204
Q

What are the 9 investigations in a full polysomnography study?

A
  1. EEG- sleep staging
  2. Video
  3. Audio
  4. Thoracic and abdominal bands
  5. Position
  6. Flow
  7. Oxygen Saturations
  8. Limb leads
  9. Snore
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205
Q

What are the 4 advantages of a full polysomnography study?

A
  1. Correct patient
  2. Accurate assessment of sleep efficiency
  3. Sleep staging via EEG
  4. Parasomnic activity- acting out dreams, sleep talking
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206
Q

What does TOSCA stand for?

A

Transcutaneous Oxygen Saturations & Carbon dioxide Assessment (home or inpatient)

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207
Q

What is apnoea?

A
  • The cessation, or near cessation, of airflow

- 4% oxygen desaturation, lasting ≥ 10 secs

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208
Q

What is hypopnoea?

A

Reduction of airflow to a degree insufficient to meet the criteria for an apnoea

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209
Q

What is respiratory effort related arousals?

A

Arousals associated with a change in airflow that does not meet the criteria for apnoea or hypopnoea

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210
Q

How is Apnoea-Hypopnoea Index (AHI) calculated?

A

Adding the number of apnoeas & hypopnoeas & dividing by the total sleep time (in hours)

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211
Q

What is Oxygen desaturation index (ODI)?

A

The number of times per hour of sleep that the SpO2 falls ≥ 4% from baseline

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212
Q

What Apnoea/Hypopnoea Index (AHI) is diagnostic of obstructive sleep apnoea?

A

=> 15
OR
5-15 with compatible symptoms

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213
Q

Describe the ranges of Apnoea/Hypopnoea Index (AHI) and how they correlate to the severity of obstructive sleep apnoea?

A
  • AHI < 5 Normal
  • AHI 5-15 Mild
  • AHI 16-30 Moderate
  • AHI >30 Severe
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214
Q

What is the aim of obstructive sleep apnoea syndrome treatment?

A

Improve daytime somnolence & QOL

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215
Q

What are the 4 means of treatment for obstructive sleep apnoea syndrome?

A
  1. Explain OSAS
  2. Weight loss
  3. Avoid triggering factors- alcohol
  4. Treat underlying conditions- tonsils, hypothyroidism, nasal obstruction
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216
Q

What does CPAP stand for?

A

Continuous positive airways pressure

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217
Q

Describe Continuous positive airways pressure (CPAP)?

A
  • Mask over the nose gently directs air into the throat to keep the airway open
  • Splints airway open
  • Stops snoring
  • Stops sleep fragmentation
  • Improves daytime sleepiness +QOL
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218
Q

What is the compliance of Continuous positive airways pressure (CPAP)?

A

> 4hrs for >70% days

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219
Q

What are the different types of CPAP?

A
  • Fixed vs Autoset CPAP

- Nasal vs Full Face Mask

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220
Q

How would you follow up CPAP treatment?

A

Annually by physiology once CPAP established

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221
Q

Describe the treatment of OSAS (obstructive sleep apnoea syndrome)?

A
  1. Mandibular Advancement Device
  2. Mild-moderate OSAS unable to tolerate CPAP
  3. Needs good dentition
  4. Maxillary-mandibular surgery
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222
Q

What 2 cases of OSAS would need Maxillary-mandibular surgery?

A
  1. Problematic patients

2. Severe retrognathia/micrognathia

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223
Q

Decrease sleep position trainers?

A
  • Supine OSA
  • Vibration when on back
  • Weeks to change sleeping position
  • Appropriate in few patients with Supine OSA
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224
Q

What 6 consequences can occur due to untreated OSAS?

A
  1. Hypertension
  2. Right heart strain
  3. Cardiovascular disease
  4. Increased risk of CVA
  5. Increased accidents at work/poor concentration
  6. Increased road traffic accidents
225
Q

How likely is untreated OSAS going to cause road traffic accidents?

A

4x more likely

226
Q

What is the BTS position statement on driving & OSA/OSAS?

A
  • OSA without daytime somnolence, do not need to stop driving
  • OSAS (DTS) is likely to impair driving, inform DVLA on diagnosis
  • OSAS can hold licence if compliant with treatment & reduced DTS
  • CAT 2 licence require ongoing monitoring by DVLA with regards to treatment complaince
227
Q

What is the standard investigation for Obstructive sleep apnoea?

A

Limited sleep study

228
Q

What is the main treatment for obstructive sleep apnoea syndrome?

A

CPAP

229
Q

What is the definition of a pneumothorax?

A

Air within the pleural cavity

230
Q

Describe the pleural cavity?

A
  • Usually a potential space
  • Negative intrapleural pressure: opposing forces of chest wall (outwards) & lung (inwards)
  • Any breach of the pleural space leads to collapse of the elastic lung
231
Q

What are 3 causes of a pneumothorax?

A
  1. Traumatic
  2. Iatrogenic
  3. Spontaneous
232
Q

Give 2 examples of a traumatic pneumothorax?

A
  1. Stabbing

2. Fractured rib

233
Q

Give 3 examples of an Iatrogenic pneumothorax?

A
  1. CT guided lung biopsy
  2. Transbronchial lung Biopsy
  3. Pleural aspiration
234
Q

Give 2 examples of a spontaneous pneumothorax?

A
  1. Primary- young patient, no underlying lung disease

2. Secondary- underlying lung disease (COPD, cystic fibrosis)

235
Q

Descrive a tension pneumothorax?

A
  • Medical emergency
  • ‘One way valve’ leads to increased intrapleural pressure
  • Venous return impaired, cardiac output and blood pressure fall
236
Q

What would happen to a tension pneumothorax if there was no intervention?

A

Pulseless electrical activity (PEA) cardiac arrest

237
Q

What is the immediate management of a tension pneumothorax?

A

Insert venflon 2nd intercostal space midclavicular line to relieve pressure

238
Q

What are 4 risk factors for a spontaneous pneumothorax?

A
  1. Smoking
  2. Male gender
  3. Height
  4. Underlying lung disease (secondary)
239
Q

What is the % recurrence rate after 1st episode of a spontaneous pneumothorax?

A

40-50%

240
Q

Describe the pathophysiology of primary pneumothorax?

A
  • Development of subpleural blebs/ bullae at lung apex
  • Spontaneous rupture leads to tear in visceral pleura
  • Air flows from airways to pleural
    space (pressure gradient)
  • Elastic lung then collapses
241
Q

What can additionally occur in the pathophysiology of a primary pneumothorax?

A

Diffuse, microscopic emphysema below the surface of the visceral pleura

242
Q

Describe the pathophysiology of secondary pneumothroax?

A
  • Inherent weakness in lung tissue (eg emphysema)
  • Increased airway pressure (eg asthma, ventilated patient)
  • Increased lung elasticity (eg pulmonary fibrosis)
243
Q

Describe the presentation of a secondary pneumothorax?

A

Patient is generally much more symptomatic (poor underlying lung function)

244
Q

Describe the management of a secondary pneumothorax?

A
  • Management more complex, prognosis less good

- More likely to require intervention

245
Q

List the 3 symptoms of a pneumothorax?

A
  1. Pleuritic chest pain
  2. Breathlessness (can be minimal if primary)
  3. Respiratory distress (especially if secondary)
246
Q

List the 4 signs of a pneumothorax?

A
  1. Reduced air entry on affected side
  2. Hyper-resonance to percussion
  3. Reduced vocal resonance
  4. Tracheal deviation if tension (+/- circulatory collapse)
247
Q

What are the 3 potential differential diagnosis for a pneumothorax?

A
  1. Pulmonary thromboembolism (PTE)
  2. Musculoskeletal pain
  3. Pleurisy/ pneumonia
248
Q

What 2 imaging techniques would you use for a pneumothorax?

A
  1. CXR

2. CT chest

249
Q

Why is the size of pneumothorax less important than symptoms?

A
  • Small pneumothorax very symptomatic if bad COPD

- Can tolerate complete lung collapse very well if healthy

250
Q

What does 2cm rim of air at the axilla equate to?

A

50% volume

251
Q

What is defined as a small/large pneumothorax?

A
  • <2cm= Small

- >2cm= Large

252
Q

What are the 3 options for pneumothorax management?

A
  1. Observation (serial CXR) if small or not very symptomatic- can be as outpatient
  2. Aspiration (small bore catheter 2nd intercostal space midclavicular line- aspirate air with syringe/ 3 way tap)
  3. Intercostal drain with underwater seal
253
Q

What 4 interventions are done if a drain fails to work in a pneumothorax?

A
  1. VATS (Video Assisted Thoracic Surgery)- considered if not resolved in 5 days
  2. Staple blebs
  3. Talc pleurodesis
  4. Pleural abrasion/ stripping
254
Q

What does Talc pleurodesis cause?

A

Causes inflammatory reaction & pleural adhesion, highly effective

255
Q

When would surgical pleurodesis be considered?

A

If 2nd pneumothorax on same side, 1st contralateral event

256
Q

After a spontaneous pneumothorax has resolved on CXR, how long should the patient wait before flying?

A

=> 7 days

257
Q

After a spontaneous pneumothorax has resolved on CXR, how long should the patient wait before diving?

A

Should not dive again (too high a risk of recurring pneumothorax)

258
Q

Describe the prevalence of lung cancer?

A
  • 3rd most common cancer in the UK (2015)
  • Accounts for 13% of all new cancer cases
  • In men 2nd commonest after prostate cancer
  • In women 2nd commonest after breast cancer
  • > 44% of lung cancer occurs in the over 75s, highest in 85-89year olds
259
Q

Where in the UK has the highest incidence rates of lung cancer?

A

Scotland (3rd higher in Glasgow due to the high smoke prevalence)

260
Q

Describe lung cancer prognosis statistics?

A
  • Long term survival from lung cancer is poor (5%)

- Lung cancer is usually caused by smoking & is therefore in almost 90% of cases a preventable disease

261
Q

Describe lung cancer mortality rates?

A
  • 50% of the deaths occur in over 75
  • Overall last decade mortality decreased by 6% (16% decrease in males & 6% increase in females)
  • More common in people living in deprived areas
  • Commonest cause of death from malignant disease
262
Q

Describe the survival rates of lung cancer?

A
  • Lowest survival outcome of any cancer
  • Survival is increasing
  • ~1/3 of people diagnosed with lung cancer survive at least 1 year after diagnosis
  • 5% of people diagnosed with lung cancer survive at least 10 years after diagnosis
263
Q

What is 90% of lung cancer due to?

A

Life style

264
Q

What is the main avoidable risk for lung cancer (89% of cases)?

A

Smoking- has the strongest link to squamous & small cell

265
Q

Describe the smoking risks of lung cancer?

A
  • <5% are life long non-smokers
  • 10-20 cig/day : 30x risk
  • 60 cig/day : 60x risk
266
Q

List 7 other risk factors for lung disease?

A
  1. Environmental tobacco smoke
  2. Ionising radiation- radon, uranium
  3. Air pollution
  4. Asbestos
  5. Fibrosing conditions of lung
  6. Human papilloma virus
  7. Hereditary (polymorphisms in cytochrome p450)
267
Q

List the 6 signs & symptoms of lung cancer?

A
  1. Cough
  2. Haemoptysis
  3. Shortness of Breath
  4. Chest pain
  5. Weight loss/Anorexia
  6. General malaise
268
Q

What are the 3 main signs & symptoms for a central lung cancer?

A
  1. Haemoptysis
  2. Bronchial obstruction- SOB, retention pneumonia
  3. Cough
269
Q

What are the 2 signs & symptoms for a peripheral lung cancer?

A
  1. May have few symptoms

2. Pain if pleura or chest wall involved

270
Q

Where are 6 locations for lung cancer to spread locally?

A
  1. Pleura
  2. Hilar lymph nodes
  3. Adjacent lung tissue
  4. Pericardium
  5. Mediastinum
  6. Pancoast tumour
271
Q

What can local lung cancer spread to pleura cause?

A

Haemorrhagic effusion

272
Q

What may lung cancer spread to adjacent lung tissue involve?

A

Large blood vessel leading to haemoptysis

273
Q

What can pericardial local lung cancer spread cause?

A

Pericardial effusion with subsequent involvement of pericardium

274
Q

What 3 structures can local mediastinum spread of lung cancer affect?

A
  1. Superior vena caval obstruction
  2. Recurrent laryngeal nerve
  3. Phrenic nerve
275
Q

What can pancoast tumour spread of lung cancer cause?

A
  • Involvement of brachial plexus giving sensory & motor symptoms
  • Horner’s syndrome/Oculosympathetic palsy (cervical sympathetic chain)
276
Q

What does local spread of lung cancer causing SVC obstruction lead to?

A
  • Oedema of face & arms
  • Raised JVP
  • Dilated veins on chest wall
  • Plethoric face
  • Headache worse on stooping
277
Q

What does local spread of lung cancer causing phrenic nerve paralysis lead to?

A

Diaphragmatic paralysis (the right hemidiaphragm goes up)

278
Q

What does local spread of lung cancer causing recurrent laryngeal nerve paralysis lead to?

A

Hoarseness of the voice

279
Q

What is Pancoast tumour?

A

Tumour of the pulmonary apex which can involved brachiocephalic vein, Brachial plexus subclavian etc.

280
Q

List the 3 signs & symptoms of Pancoast tumour?

A
  1. Severe pain in the shoulder or the scapula
  2. Pain in the arm & weakness of the hand on the affected side
  3. Horner’s syndrome
281
Q

Describe Horner’s syndrome?

A
  • Due to invasion of cervical sympathetic chain (can be due to Pancoast tumour)
  • Ptosis
  • Enophthalmos
  • Miosis (constriction of pupil)
  • Anhydrosis
282
Q

List 2 areas that lung cancer can spread to distally?

A
  1. Haematogenous

2. Lymphatics (cervical lymph nodes)

283
Q

Describe Haematogenous distal spread of lung cancer?

A
  • Common due to invasion of pulmonary veins

- Liver, bone, brain, adrenal

284
Q

Describe Cushing’s syndrome?

A
  • ACTH secretion
  • Adrenal hyperplasia
  • Raised blood cortisol
285
Q

Describe Syndrome of inappropriate antidiuretic hormone secretion (SIADH)?

A
  • ADH secretion
  • Retention of water
  • Dilutional hyponatraemia
286
Q

What does the secretion of Parathyroid hormone related peptide (PTHrP) cause?

A
  • Osteoclast activity

- Hypercalcaemia

287
Q

What are the 3 main non-metastatic effects of lung cancer?

A
  1. ACTH secretion
  2. ADH secretion
  3. Parathyroid hormone related peptide (PTHrP) secretion
288
Q

List 6 other non-metastatic effects of lung cancer?

A
  1. Encephalopathy
  2. Cerebellar degeneration
  3. Neuropathy
  4. Myopathy
  5. Eaton Lambert myasthenia-like syndrome
  6. Cancer Associated Retinopathy
289
Q

Describe small cell lung cancer?

A

Usually advanced at diagnosis & responds to chemotherapy

290
Q

Describe non-small cell lung cancer?

A

May be localised at diagnosis & can be treated by surgery or radiotherapy

291
Q

What is the prevalence of 5 different types of lung cancers by Histology?

A
  1. Adenocarcinoma 40%
  2. Squamous cell carcinoma 30%
  3. Small cell lung carcinoma 15%
  4. Large cell carcinoma 10%
  5. Other 3%
292
Q

List 5 other histological types of lung cancers?

A
  1. Mesenchymal Tissues- inflammatory myofibroblastic tumour
  2. Salivary gland-type- adenoid cystic carcinoma
  3. Ectopic Origin- germ cell tumours
  4. Neuroendocrine cells- carcinoid
  5. Lymphatic system- lymphoma
293
Q

Why has there been a recent rise in adenocarcinoma & small cell carcinoma with fall in squamous carcinoma?

A
  • Change in smoking demographics (more women now getting lung cancer)
  • Filter tips, lower tar & nicotine
  • Deeper inhalation exposes more peripheral airways to carcinogens
294
Q

Describe the site of central lung tumours?

A

Arise in & around hilus of the lung and are usually squamous or small cell carcinomas

295
Q

What are peripheral lung tumours predominantly?

A

Adenocarcinomas

296
Q

Describe small cell carcinoma?

A
  • Most aggressive form of lung cancer
  • Metastasises early & widely
  • Often initial good response to chemotherapy, but most patients relapse
297
Q

Describe the appearance of small cell carcinoma (4)?

A
  1. Oval to spindle shaped cells
  2. Inconspicuous nucleoli
  3. Scant cytoplasm
  4. Nuclear moulding (more prominent in cytology)
298
Q

What 2 things does small cell carcinomas have in histology?

A
  1. Apoptotic bodies

2. Nuclear moulding

299
Q

List 3 non-small cell carcinomas?

A
  1. Squamous cell carcinoma
  2. Adenocarcinoma
  3. Large cell carcinoma
300
Q

Describe squamous cell carcinomas?

A
  • Tend to arise centrally from major bronchi
  • Often within dysplastic epithelium following squamous metaplasia
  • Slow growing & metastasise late therefore may be good candidate for surgery
301
Q

What 2 things may happen in squamous cell carcinomas?

A
  1. May undergo cavitation

2. May block bronchi leading to retention pneumonia or collapse

302
Q

Describe the appearance of squamous cell carcinomas?

A
  • Malignant epithelial tumour showing keratinzation &/or intercellular bridges
  • In situ squamous cell carcinoma may seen in the adjacent airway mucosa
303
Q

What does squamous tumours produce?

A

Keratin

304
Q

Describe Adenocarcinoma?

A
  • Common tumour in females
  • Seen in non-smokers (but also associated with smoking)
  • 2/3s arise in periphery sometimes in relation to scarring
305
Q

Describe the appearance of an Adenocarcinoma?

A
  • Glandular, solid, papillary or lepidic

- Mucin production

306
Q

Describe large cell carcinoma?

A
  • Usually arises centrally
  • Undifferentiated malignant epithelial tumour that lacks the cytological features of SCLC & glandular or squamous differentiation
307
Q

How do you diagnose large cell carcinoma?

A

Diagnosis of exclusion

308
Q

Describe a carcinoid tumour?

A
  • Tumour of neuroendocrine cells
  • Central or peripheral
  • Classified as Typical or Atypical
309
Q

Describe the prognosis of carcinoid tumours?

A

Can metastasize but MUCH better prognosis than other conventional lung cancers (5YS for typical 85-90%; Atypical 5YS 50-75%)

310
Q

List 3 molecular targets identified for lung cancer?

A
  1. Epidermal Growth Factor Receptor (EGFR)
  2. Echinoderm Microtubule-Associated Protein like 4-Anplastic lymphoma kinase fusion gene
  3. Immunotherapy- PDL1
311
Q

Describe the function of Epidermal Growth Factor Receptor (EGFR)?

A
  • Extracellular component is responsible for ligand binding
  • Intracellular component consists of the tyrosine kinase which is responsible for signal transduction & activates several growth pathways
312
Q

What can mutations of EGFR cause?

A

It to become constitutionally active.

313
Q

How would you test for mutations in EGFR?

A
  • Performed on biopsy or cytology specimens

- PCR or Sequencing used to look for mutations in EGFR

314
Q

What are deletions in EGFR Exon 19 commonly associated with?

A

Good response to EGFR inhibitors

315
Q

What does ALK & EML4 fusion lead to?

A

Constitutive activation of a chimeric tyrosine kinase leading to increased cell proliferation

316
Q

What drug inhibits ALK & EML4 fusion & hence inhibits cell proliferation?

A

Crizotinib

317
Q

What are 2 ways to test for ALK fusion?

A
  1. FISH

2. Immunohistochemistry for protein product

318
Q

Describe PDL1 in lung cancer?

A

PD-L1 binds to PD-1 & inhibits T cell killing of tumour cell

319
Q

What can mutated EGFR receptors (~13% in glasgow) respond to?

A

Tyrosine kinase inhibitors (ROS-1)

320
Q

What do ~3-7% of NSCLC patients have?

A

EML4-ALK gene fusions present in their tumours, which may respond to ALK-inhibitors

321
Q

What is over-expressed in 30-40% of tumours?

A

PD-L1 & may be treated with PD-L1 inhibitors

322
Q

List the 9 common sites of secondary cancers which spread to the lung?

A
  1. Breast
  2. Colorectal
  3. Kidney
  4. Head and neck
  5. Testicular
  6. Bone (osteosarcoma)
  7. Sarcomas
  8. Melanoma
  9. Thyroid
323
Q

List the 6 signs & symptoms of secondary cancer to the lungs?

A
  1. Cough
  2. Shortness of breath
  3. Frequent chest infections
  4. Haemoptysis
  5. Pain
  6. Weight loss
324
Q

What is mesothelioma?

A

Primary pleural tumour (also occurs in peritoneum, pericardium & tunica vaginalis testis)

325
Q

Describe Mesothelioma?

A
  • Almost always due to asbestos exposure
  • Very long lag period
  • Either an epithelial or sarcomatoid appearance or a mixture of both (biphasic)
326
Q

Describe a mesothelioma on CT scan?

A
  • Encases the lung

- Mass in the pleura

327
Q

What is often found in the sputum of someone with a mesothelioma?

A

Asbestos body

328
Q

What is sarcoidosis?

A

Multisystem inflammatory disease of unknown etiology that predominantly affects the lungs & intrathoracic lymph nodes

329
Q

Describe the presentation of sarcoidosis?

A
  • ~5% of cases are asymptomatic & incidentally detected by CXR
  • Presentation depends on the extent & severity of the organ involved
330
Q

List the 5 systemic symptoms that occur in 45% of sarcoidosis cases?

A
  1. Fever
  2. Anorexia
  3. Fatigue
  4. Night sweats
  5. Weight loss
331
Q

What symptoms occur in 50% of sarcoidosis patients?

A

Pulmonary, dyspnea on exertion, cough, chest pain & hemoptysis (rare)

332
Q

List the 5 clinical signs of sarcoidosis?

A
  1. Pulmonary findings
  2. Dermatological manifestations
  3. Ocular manifestations
  4. Cardiac manifestations
  5. Neurologic manifestations (rare)
333
Q

How is sarcoidosis diagnosed?

A
  • You can see on a chest X-ray & what organs are affected
  • Bronchoscopy & perhaps take a tissue biopsy
334
Q

List the 4 lung signs of sarcoidosis?

A
  1. Dyspnea
  2. Cough
  3. Vague chest discomfort
  4. Wheezing
335
Q

Describe the 4 stages of chest radiographs in patients with sarcoidosis?

A
  • Stage 1: bilateral hilar lymphadenopathy without infiltration
  • Stage 2: bilateral hilar lymphadenopathy with infiltration
  • Stage 3: infiltration alone
  • Stage 4: fibrotic bands, bullae, hilar retraction, bronchiectasis & diaphragmatic tenting
336
Q

What do/don’t the stages of lung sarcoidosis represent?

A
  • Represent radiographic patterns

- Don’t indicate disease chronicity or correlate with changes in pulmonary function

337
Q

Describe the lung histology of sarcoidosis?

A
  • Schaumann body
  • Granuloma (collection of activated macrophages)
  • Giant cell of lots of nuclei
  • Non-necrotising granulomas inflammation (giant cells)
  • Asteroid bodies (not diagnostic of sarcoidosis but its consistent with it)
338
Q

What is sarcoidosis characterised by?

A

Non-necrotising Granulomatous Inflammation

339
Q

Sarcoidosis is a diagnosis of _____?

A

Exclusion

340
Q

Describe the 2 issues with pulmonary fibrosis?

A
  1. A lot of causes for Pulmonary Fibrosis
  2. It is a difficult diagnosis to make in some cases & the whole picture has to add up: Radiology, Pathology & Clinical
341
Q

What is Idiopathic pulmonary fibrosis (IPF)?

A

Clinical manifestation or equivalent of the pathological diagnosis usual interstitial pneumonia (UIP)

342
Q

Describe the prognosis of usual interstitial pneumonia (UIP)?

A

High mortality, 50% are dead after 2 years

343
Q

What is pulmonary Fibrosis?

A

Fibrosis which is not caused by other causes & affects the respiratory apparatus of the lungs

344
Q

Describe the epidemiology of Idiopathic Pulmonary Fibrosis (IPF)?

A
  • Age > 50

- M:F - 2:1

345
Q

Describe the signs & symptoms of Pulmonary Fibrosis?

A
  • Progressive breathlessness (worse with exercise)
  • Bibasilar crackles
  • Hacking dry cough
  • Fatigue & weakness
  • Appetite & weight loss
  • Clubbing
  • PERIPHERAL Interstitial pattern
346
Q

What is the main feature of a post-mortem Idiopathic Pulmonary Fibrosis (IPF) lung?

A

Subpleural honeycombing

347
Q

List the 6 potential causes of pulmonary fibrosis?

A
  1. Occupational & Environmental- Asbestosis, Hypersensitivity Pneumonitis
  2. Drug Induced-Nitrofurantoin, Methotrexate, Cocaine
  3. Connective Tissue Diseases- Lupus, RA
  4. Primary Diseases- Sarcoidosis
  5. Idiopathic (25%)- IPF, NSIP
  6. Genetics
348
Q

How do you diagnose pulmonary fibrosis?

A

High-resolution computed tomography (HRCT) & if this shows no signs then do a biopsy (at least 3)

349
Q

What does VATS stand for?

A

Video-Assisted Thoracoscopic Surgery

350
Q

Describe the histological appearance of pulmonary fibrosis?

A
  • Fibroblastic focus is not diagnostic but a feature of UIP
  • Smooth muscle hyperplasia can occur in IUP which is a sign of long term scarring
  • Temporal heterogenity, means there are different evolutions of scar formation
  • Free radicals in the alveoli
351
Q

Describe how lung fibrosis is formed?

A

Repetitive alveolar epithelial injury –> Altered alveolar microenvironment –> Dysregulated repair, loss of epithelial cells, accumulation of mesenchymal cells –> Fibrosis

352
Q

What is Extrinsic Allergic Alveolitis (EAA)/ Henoch Schönlein Purpura (HSP)?

A
  • Immunologically mediated inflammatory reaction in the alveoli & in the bronchioles
  • It is NOT atopy, It is a T-cell mediated response
353
Q

List the 4 causes of Extrinsic Allergic Alveolitis (EAA)/ Henoch Schönlein Purpura (HSP)?

A
  1. Organic dusts (<5µm)
  2. Moulds
  3. Foreign proteins (animals)
  4. Some chemicals (lots of others)
    - Often heavy, repeated exposure, most often at the work place
354
Q

List 10 examples of Extrinsic Allergic Alveolitis (EAA)?

A
  1. Farmer’s lung
  2. Saw mill worker’s lung
  3. Bird fancier’s lung
  4. Mushroom workers lung
  5. Malt workers lung
  6. Humidifier lung
  7. Cheese washer’s lung
  8. Suberosis
  9. Diisocyanate lung
  10. Hard metal worker’s lung
355
Q

List the 5 symptoms of Extrinsic Allergic Alveolitis (EAA)/ Henoch Schönlein Purpura (HSP)?

A
  1. Flu-like illness
  2. Cough
  3. High fever, chills
  4. Dyspnea, chest tightness
  5. Malaise
  6. Myalgia
356
Q

When do symptoms occur in Extrinsic Allergic Alveolitis (EAA)/ Henoch Schönlein Purpura (HSP)?

A

4-8 hours after exposure

357
Q

List the 5 symptoms in CHRONIC Extrinsic Allergic Alveolitis (EAA)/ Henoch Schönlein Purpura (HSP)?

A
  1. Dyspnea in strain
  2. Sputum production
  3. Fatigue
  4. Anorexia
  5. Weight loss
358
Q

Describe the chest X ray appearance of acute Henoch Schönlein Purpura (HSP)?

A
  • Numerous poorly defined small ( < 5 mm) opacities in both lungs
  • Sometimes sparing of apices & bases
  • Airspace disease: usually seen asground glass opacities
  • Fine reticulation may also occur zonal distribution
359
Q

Describe the pathological appearance of Extrinsic Allergic Alveolitis (EAA)/ Henoch Schönlein Purpura (HSP)?

A
  • Bronchiolocentric pattern
  • Non-necrotising granulation
  • Foamy macrophages in alveolar spaces
  • Chronic interstitial inflammation (alveoli)
  • Organising pneumonia
360
Q

Sarcoidosis the inflammation is in the ___________, in the hypersensitivity pneumonitis it’s in the __________?

A
  1. Interstitium

2. Airspaces

361
Q

What 7 things do you give in life threatening acute exacerbation of asthma?

A
  1. High flow oxygen
  2. Nebulised bronchodilators (500mg salbutamol, 500mcg ipatropium bromide)
  3. Oral prednisolone 40mg
  4. Oral doxycycline 200mg
  5. IV magnesium 2g
  6. Discussion with ITU
362
Q

What would you consider giving for life threatening acute exacerbation of asthma?

A

IV aminophylline infusion

363
Q

What is the normal dose of amoxicillin?

A

500mg orally 8 hourly/ 1g intravenously 8 hourly

364
Q

What is the mechanism of action of amoxicillin?

A

Inhibits bacterial cell wall synthesis

365
Q

What are 2 important Pharmacokinetics / Pharmacodynamics of amoxicillin?

A
  1. Beta-lactamase production is the most common mechanism of resistance
  2. Predominantly renally excreted
366
Q

What is the normal dose of Clarithromycin?

A

500 mg orally 12 hourly

367
Q

What is the mechanism of action of Clarithromycin?

A

Bacteriostatic drug inhibiting protein synthesis

368
Q

What are 3 side effects of Clarithromycin’s mechanism of action?

A
  1. Rapidly absorbed orally- can cause phlebitis IV so avoid
  2. Hepatic metabolism- caution in liver failure & reduce dose in significant renal impairment
  3. Inhibits CYP450 (theophylline warfarin, carbamazepine, digoxin, phenytoin, simvastatin (myopathy))
369
Q

What should you be cautious about when prescribing Clarithromycin?

A

QT prolongation

370
Q

What is the normal dose of Doxycycline?

A

200mg then 100mg daily (oral)

371
Q

Describe Doxycycline?

A

Tetracycline, broad range of activity, long half-life

372
Q

What is the mechanism of action of Doxycycline?

A
  • Bacteriostatic drug, inhibits addition of amino acids to growing peptide
  • Well absorbed orally
373
Q

When should you be cautious in prescribing Doxycycline?

A
  • Patients with hepatic impairment

- Chelates calcium so avoid in young children & pregnancy

374
Q

What is the normal dose for co-amoxiclav?

A

625mg orally 8 hourly/ 1.2g intravenously 8 hourly

375
Q

Describe the mechanism of action of clavulanic acid (in co-amoxiclav)?

A

Irreversible inhibitor of β-lactamases – prevents cleavage of amoxicillin

376
Q

When should you be caution in prescribing co-amoxiclav?

A

Predominantly renally excreted therefore reduce dose in severe renal impairment

377
Q

Describe the mechanism of action of corticosteroids?

A

Bind to activated glucocorticoid receptors to suppress multiple pro-inflammatory genes that are activated in asthmatic airways by reversing histone acetylation

378
Q

What are the 3 indications for corticosteroid prescription?

A
  1. Asthma
  2. COPD with recurrent exacerbations
  3. Exacerbations of asthma/COPD
379
Q

List the 13 side effects of corticosteroids (there are many others)?

A
  1. Diabetes
  2. Osteoporosis
  3. Hypertension
  4. Muscle wasting
  5. Peptic ulceration
  6. Cataracts
  7. Cushing’s syndrome
  8. Adrenal suppression
  9. Acute pancreatitis
  10. Hyperlipidaemia
  11. Increased appetite
  12. Salt & water retention
  13. Immune suppression
380
Q

Describe the mechanism of action of Bronchodilators: 𝛃2 agonist?

A
  • Higher specificity for pulmonary (𝛃2) receptors vs. cardiac (𝛃1) receptors
  • Stimulate adenyl cyclase to increase intracellular cAMP –> relaxation of bronchial smooth muscle
381
Q

What are 2 indications for Bronchodilators: 𝛃2 agonist?

A
  1. Treatment of asthma

2. Treatment of COPD

382
Q

List 9 side effects of Bronchodilators: 𝛃2 agonist?

A
  1. Tremor
  2. Hypokalaemia
  3. Hyperglycaemia
  4. Hypomagnesaemia
  5. Flushing
  6. Tachycardia
  7. Arrhythmias
  8. Headache
  9. Muscle cramps
383
Q

What are 2 examples of short acting Bronchodilators: 𝛃2 agonist?

A

Salbutamol & Terbutaline (elimination half-life ~3 – 5 hours)

384
Q

What are 4 examples of long acting Bronchodilators: 𝛃2 agonist?

A
  1. Salmeterol
  2. Formoterol
  3. Vilanterol
  4. Indacaterol
385
Q

List 4 routes of administration for salbutamol?

A
  1. Inhaled (preferred)
  2. Nebulised (if severe)
  3. Oral
  4. IV
386
Q

What is the mechanism of action of Bronchodilators: Anti-muscarinics?

A

Inhibition of cholinergic M1 & M3 receptors in lung –> reduction in cGMP & inhibition of parasympathetic-mediated bronchoconstriction

387
Q

List the 5 side effects of bronchodilators: Anti-muscarinics?

A
  1. Blurred vision
  2. Dry mouth
  3. Urinary retention
  4. Nausea
  5. Constipation
388
Q

What may nebulised ipatropium precipitate?

A

Acute angle closure glaucoma – use a mouthpiece not a mask

389
Q

Give an example of a short acting bronchodilators: Anti-muscarinics?

A

Ipatropium bromide

390
Q

Give 3 examples of long acting bronchodilators: Anti-muscarinics?

A
  1. Tiotropium
  2. Glycopyrronium
  3. Umeclidinium
391
Q

How are bronchodilators: Anti-muscarinics excreted?

A

Renally

392
Q

What is the mechanism of action for Bronchodilators: Methylxanthines?

A
  • Non-selective inhibition of phosphodiesterase –> increased intracellular cAMP –> bronchial smooth muscle relaxation
  • Immunomodulatory action: improved mucociliary clearance & anti-inflammatory effect
393
Q

Give 2 examples of Bronchodilators: Methylxanthines?

A
  1. Aminophylline

2. Theophylline

394
Q

What is an indication for Bronchodilators: Methylxanthines?

A

Adjunct to inhaled therapy in asthma/intravenous infusion in severe exacerbations of asthma

395
Q

List 6 side effects of Bronchodilators: Methylxanthines?

A
  1. GI upset
  2. Palpitations
  3. Tachycardia/arrhythmias
  4. Headache
  5. Insomnia
  6. Hypokalaemia
396
Q

What are important Pharmacokinetics / Pharmacodynamics for Bronchodilators: Methylxanthines?

A

Time to steady state: 2- 3 days, plasma theophylline levels at 5 days/3 days after dose adjustment

397
Q

What is the problem with Bronchodilators: Methylxanthines?

A

Narrow therapeutic window: 10 – 20mg/L so drug monitoring: 4 – 6 hours post-dose

398
Q

What can Bronchodilators: Methylxanthines toxicity do?

A
  1. Severe vomiting
  2. Hypokalaemia/hypocalcaemia
  3. Seizures
  4. Arrhythmias
  5. Hypotension
  6. Weight-based dosing
399
Q

Where is Bronchodilators: Methylxanthines metabolised?

A

Liver- caution in liver disease & with concomitant use of enzyme inducers (rifampicin) and inhibitors (clarithromycin, ciprofloxacin)

400
Q

What increases theophylline (Bronchodilators: Methylxanthines) clearance?

A

Smoking

401
Q

Give 3 examples of LABA/LAMA combination inhalers?

A
  1. Anoro ® Ellipta (Umeclidinium/Vilanterol)
  2. Ultibro ® Breezhaler (Glycopyrronium/Indacaterol)
  3. Duaklir ® Genuair (Aclidinium/Formoterol)
402
Q

Give 4 examples of LABA/ICS combination inhalers?

A
  1. Relvar ® Ellipta (Fluticasone/Vilanterol)
  2. Seretide ® Accuhaler/Evohaler (Fluticasone/Salmeterol)
  3. Symbicort ® Turbohaler (Budesonide/Formoterol)
  4. Fostair MDI (Beclometasone/Formoterol)
403
Q

Give 2 examples of Leukotriene receptor antagonists used in asthma?

A
  1. Montelukast

2. Zafirlukast

404
Q

What is the mechanism of action of Leukotriene receptor antagonists?

A

Bind with high affinity to cysteinyl leukotriene receptor (CysLT1) inhibiting action of LTD4 in smooth muscle cells of the airway and airway macrophages –> reduced airway oedema & smooth muscle contraction

405
Q

What are Leukotriene receptor antagonists useful for?

A

Prophylaxis of exercise-induced asthma, allergic rhinitis

406
Q

Leukotriene receptor antagonists have a ___ half-life?

A

Short

407
Q

Describe Omalizumab (Leukotriene receptor antagonists)?

A
  • Monoclonal anti-IgE antibody
  • Severe persistent allergic asthma
  • Subcutaneous injection every 4 weeks
  • Dose based on IgE & weight
  • Risk of severe hypersensitivity reaction
408
Q

Describe Mepolizumab (Leukotriene receptor antagonists)?

A
  • Anti-IL5 monoclonal antibody
  • Reduces circulating eosinophils
  • Severe refractory eosinophilic asthma
  • Subcutaneous injection every 4 weeks
  • Headaches commonly reported
409
Q

Describe the GOLD COPD Guideline?

A

Spirometrically confirmed diagnosis (post-bronchodilator FEV1/FVC < 0.7) –> Assessment of airflow limitation –> Exacerbation history –> Assessment of symptoms/risk of exacerbations (A,B,C,D)

410
Q

What is Roflumilast drug?

A

Selective inhibitor of phosphodiesterase-4

411
Q

What is the mechanism of action of Roflumilast?

A

Inhibits hydrolysis of cAMP in inflammatory cells –> increased intracellular cAMP –> reduced release of pro-inflammatory mediators & cytokines

412
Q

How is Roflumilast metabolised?

A

By cytochrome P450

413
Q

What is the indication for Roflumilast?

A

Reduction in exacerbations of COPD

414
Q

What is the mechanism of action of Azithromycin?

A

Macrolide antibiotic with immunomodulatory & anti-inflammatory effects- inhibition of pro-inflammatory AP-1, NFκB & mucin release

415
Q

What is the indication for Azithromycin?

A

Reduction in exacerbations of COPD

416
Q

What is the mechanism of action of Carbocisteine?

A

Increases concentrations of sialomucins & reduces concentrations of fucomucins resulting in reduced sputum viscosity

417
Q

What is the indication for Carbocisteine?

A

Reduction in exaerbations of COPD

418
Q

What is Dermatophytes?

A

Fungi that cause common infections of skin, nails & hair

419
Q

Describe Dermatophytes infections?

A
  • Do not colonise ‘live’ tissues, instead keratinised areas such as nails & outer skin
  • Healthy & immunocompromised infected
420
Q

What are 3 virulence factors for Dermatophytes?

A

Keratinases, elastase & other proteinases

421
Q

What are Dermatophytes infections also known as?

A
  • Ringworm

- Tinea

422
Q

When would you treat dermatophytes infection with oral medication?

A
  • Severe infections, nail infections
  • Topical medication has not worked
  • Adults only
423
Q

Give 4 examples of active ingredients for treating dermatophytes infection?

A
  1. Terbinafine (Lamisil®)
  2. Itraconazole
  3. Ketoconazole
  4. Miconazole
424
Q

Give 3 examples of systemic fungal infections & their causes?

A
  1. Fungal meningitis- Cryptococcus neoformans
  2. Aspergillosis of the lungs- Aspergillus fumigatus
  3. Pneumocystis pneumonia- Pneumocystis jiroveci
425
Q

Who get systemic fungal infections?

A

Only immunocompromised

426
Q

Describe Cryptococcus neoformans?

A
  • Inhaled opportunistic pathogen
  • Encapsulated yeast
  • Contracted from environment, e.g. pigeon droppings
427
Q

What is often a secondary infection with HIV?

A

Crytococcosis of lungs, & meningitis

428
Q

What is the treatment of Cryptococcus neoformans infection?

A
  • 2 weeks of i.v. Amphotericin B for meningitis

- Fluconazole or flucytosine (non-CNS)

429
Q

What are 3 types of aspergillum fumigatus infections?

A
  1. Allergic bronchopulmonary aspergillosis (ABPA)
  2. Invasive pulmonary aspergillosis (IPA)
  3. Aspergilloma
430
Q

Describe Allergic bronchopulmonary aspergillosis (ABPA)?

A
  • Allergic reaction to the fungal infection
  • Association with cystic fibrosis, asthma
  • Prednisone (anti-allergic agent)
431
Q

Describe Invasive pulmonary aspergillosis (IPA)?

A
  • Becomes systemic & spreads throughout the body
  • Common in immunocompromised
  • Treatment: voriconazole; Amphotericin B
432
Q

Describe Aspergilloma?

A
  • Fungal ball that develops in an area of past lung disease or lung scarring
  • e.g. tuberculosis or lung abscess
  • No treatment unless bleeding occurs: surgery
433
Q

What is Pneumocystis jiroveci?

A

Common environmental fungus

434
Q

What can Pneumocystis jiroveci cause?

A

Pneumonia (fever, cough, shortness of breath, rapid breathing)

435
Q

How do you treat Pneumocystis jiroveci?

A

Trimethoprim-sulfamethoxazole

436
Q

What is the largest class of antifungal agents?

A

Imidazole, triazole, & thiazole antifungals

437
Q

Give 8 examples of Imidazole, triazole, & thiazole antifungals?

A
  1. Miconazole (Micatin® or Daktarin®)
  2. Ketoconazole (Nizoral, Fungoral and Sebizole®)
  3. Clotrimazole (Lotrimin, Lotrimin AF and Canesten)
  4. Econazole
  5. Isoconazole
  6. Fluconazole
  7. Itraconazole
  8. Abafungin
438
Q

What are azoles?

A

Inhibitors of 14-methylsterol α-demethylase which produces ergosterol

439
Q

Describe ergosterol?

A
  • Essential component of the fungal plasma membrane
  • Does not occur in animal or plants cells
  • Equivalent of cholesterol in yeast, fungi
440
Q

What does Terbinafine inhibit?

A

Squalene 2,3-epoxidase

441
Q

What does Azoles inhibit?

A

14-methylsterol α-demethylase

442
Q

What does Ketoconazole inhibit?

A

1 enzyme in ergosterol synthesis

443
Q

What is the drawback of Ketoconazole?

A

Cross- resistance

444
Q

Why are sterols, such as cholesterol, so important?

A

They insert themselves into the lipid bilayer & are essential for its proper functioning & viscosity

445
Q

What does Amphotericin B exploit?

A
  • Ergosterol / cholesterol difference

- Presence of ergosterol (hydrophobic side interacts with ergosterol)

446
Q

What does binding of Amphotericin B to ergosterol cause?

A

Intercalation of cell membrane (pore in fungal membranes) & leakage of intracellular cations & eventual cell death

447
Q

What is ambisome?

A

Liposome formulation with amphotericin B molecules

448
Q

What are the 2 benefits of ambisome?

A
  1. Improved delivery

2. Reduced Toxicity

449
Q

What does the mediastinum consist of?

A

Blood vessels, trachea, oseophagus, T duct & phrenic nerves, Thymus (8mm lobe young adults, 5mm > 50yrs)

450
Q

What are the 3 lung fissures?

A
  1. Major
  2. Minor
  3. Azygous
451
Q

What lung hila is higher up?

A

Left higher than right

452
Q

What is the size of lung paraspinal lines?

A

<10 mm

453
Q

What is mediastinal drift associated with?

A

Collapse/Consolidation

454
Q

What is the mediastinum best visualised on?

A

CT

455
Q

What is the main rule for assessing the mediastinum on imaging?

A

2 vessels in front (veins) & 3 arteries behind

456
Q

Describe the aorta on a chest CT?

A
  • Ascending aorta in front

- Descending aorta behind

457
Q

What are small dots on a chest CT usually?

A

Lymph nodes (normal)

458
Q

How big should lymph nodes be?

A

<1cmn

459
Q

What 4 disease cause bilateral hilar adenopathy?

A
  1. Sarcoidosis
  2. Lymphoma
  3. TB
  4. Malignancy
460
Q

Describe a mediastinal lymphoma on CXR?

A

Wide ascending aorta

461
Q

Does lobar collapse normally cause mediastinal shift?

A

NO

462
Q

What are the 4 CXR signs of right UL collapse?

A
  1. Opacification right upper zone
  2. Displacement of the horizontal fissure superiorly
  3. Bulging of fissure medially
  4. Trachea displaced to right
463
Q

What is Golden’s reverse’s sign?

A

Bulging of fissure medially

464
Q

What should you always suspect when there is a collapsed lung/lobe?

A

Tumour but other causes are possible

465
Q

What 5 investigations would you do for a suspected collapsed lung/lobe?

A
  1. History
  2. Examination
  3. Bloods
  4. CT
  5. Bronchoscopy
466
Q

What are 4 CXR signs of left UL collapse?

A
  1. Opacification left upper zone
  2. Displacement of the oblique fissure superiorly
  3. Bulging of fissure medially
  4. Trachea displaced to left
467
Q

What may be seen in a CXR of left UL collapse?

A

Veil like opacification of left hemithorax & aereated left apex due to expanded left lower lobe +/- elevated left hemidiaphram

468
Q

What are 4 CXR signs of left LL collapse?

A
  1. Wedge triangular opacification behind the left heart border “sail boat sign”
  2. Displacement of the left hilum inferiorly
  3. Obliteration of the left hemidiaphragm
  4. Hyperlucent remaining left lung
469
Q

What are 4 causes of a hyperlucent lung?

A
  1. Ring shadows- bullae
  2. Technical causes- rotation
  3. Chest wall/pleural abnormalities
  4. Vascular e.g. PTE
470
Q

What can appear like a pneumothorax on CXR?

A

Skin fold

471
Q

What is the main cause of a hyper lucent lung with mediastinal shift?

A

Pneumothorax (air in pleural space)

472
Q

What are 4 types of pneumothorax?

A
  1. Simple
  2. Hydro
  3. Haemo
  4. Pyo
473
Q

What is a pneumothorax usually due to?

A

Spontaneous rupture of pleural bleb

474
Q

What should you identify on a CXR of pneumothorax?

A

Pleural line (visceral)

475
Q

What are 4 difficulties of diagnosing pneumothorax on a CXR?

A
  1. Bullae
  2. Clothing
  3. Tubes
  4. Skin folds
476
Q

What may be helpful when diagnosing a pneumothorax?

A

Expiratory film

477
Q

Describe a pneumothorax on a supine film?

A
  • Deep costophrenic angle
  • Increased clarity of mediastinual border
  • Depression of diaphragm
  • Visualisation of undersurface of the heart
478
Q

List the 9 causes of a pneumothorax?

A
  1. Trauma- stab, iatrogenic, rib fracture
  2. Spontaneous
  3. Ventilation
  4. Pulmonary disease- fibroses
  5. Asthma
  6. Infections- TB, sepsis, septic infarct
  7. Malignancy- metasatic sarcoma
  8. Pneumomediastium- ruptured oesophagus, tracheostomy
  9. Obscure- Endometriosis
479
Q

List the 6 radiological signs on the CXR for a pneumothorax?

A
  1. Depression of the left hemidiaphragm
  2. Tracheal displacement
  3. Hyperlucency of the left hemithorax
  4. Small left basal pleural effusion
  5. Displacement of the heart to the right
  6. Pleural line or completely collapsed lung
480
Q

List 5 complications of a pneumothorax?

A
  1. Haemothorax
  2. Tension
  3. Adhesions
  4. Delayed expansion adhesions, airways obstruction
  5. Re expansion oedema
481
Q

What is a pleural effusion?

A
  • Fluid in the pleural space

- Normally fluid generated by parietal, absorbed by visceral

482
Q

What can lateral decubitas film detect in a pleural effusion?

A

50-10ml fluid

483
Q

What are the 5 types of fluid causing a pleural effusion?

A
  1. Transudate
  2. Exudate
  3. Blood- Haemothorax
  4. Chyle- Chylothorax
  5. Mixed
484
Q

What is the most common cause of a pleural effusion?

A

Cardiac failure

485
Q

List 9 causes of pleural effusions?

A
  1. Hypoproteinaemia- cirrhosis
  2. Cardiovascular- CCF, constrictive pericarditis
  3. Neoplasm
  4. Infection
  5. Trauma
  6. Thromboembolism
  7. Inhalation- asbestos
  8. Collagen vascular disease- SLE, RA
  9. Subdiaphragmatic disease- pancreatitis, subphrenic abscess
486
Q

What are the 5 most likely causes of a massive pleural effusion?

A
  1. Malignant disease
  2. Heart failure
  3. Cirrhosis
  4. TB
  5. Empyema
  6. Trauma
487
Q

What are 8 causes of an opacification of the hemithorax (half of the thorax)?

A
  1. Pleural effusion
  2. Consolidation
  3. Collapse
  4. Massive tumour
  5. Fibrothorax
  6. Combination of above
  7. Pneumonectomy
  8. Lung agenesis
488
Q

What are 5 CXR signs for a pleural effusion?

A
  1. Lat decubitas most sensitive- 5mls
  2. PA CXR; 200mls +
  3. Blunting costo phrenic angle & meniscus sign
  4. Supine film; hazy opacification & visualised vascular markings
  5. Massive effusion with contralateral shift
489
Q

What can massive effusions cause occasionally?

A

Diaphragmatic inversion, more common on left

490
Q

What is Subpulmonary effusion?

A
  • Free fluid collects initially under lung

- When >2-300ml becomes generalised

491
Q

Describe the CXR of a Subpulmonary effusion?

A
  • High hemidiaphragm (appears more opaque)

- Lateral peak to contour

492
Q

How is a subpulmonary effusion confirmed?

A

Lateral decubitus film

493
Q

What are 4 other investigations for a pleural effusion?

A
  1. Move fluid e.g. supine lat decubitas
  2. Post aspiration of fluid analysis
  3. Post aspiration film
  4. CT
494
Q

Where can fluid be loculated in a pleural effusion?

A
  1. Fissures- visceral/parietal

2. Chest wall- visceral/parietal

495
Q

Describe Fissural pleural effusion fluid?

A
  • Especially heart failure- phantom tumour
  • PA thin or mass like
  • Lateral: sharp margins, biconvex with tail along fissure
496
Q

Describe Chest Wall pleural effusion fluid?

A

PA pleural shadow with one edge sharp & one that fades

497
Q

What moves & what does not in the mediastinum?

A

Fluid moves, parenchymal pathology does not

498
Q

Describe a Haemothorax?

A
  • Identical to all pleural collections
  • Trauma commonest
  • Also seen in leaking aortic aneurysm, pneumothorax or bleeding tendency
499
Q

Describe the appearance of a Chylothorax?

A
  • Right sided with low thoracic pathology

- Left sided with high lesions

500
Q

What are 5 causes of Chylothorax?

A
  1. Trauma
  2. Tumour
  3. Inflammatory filariais- TB
  4. Primary lymphatic- lymphangioma, lymphangiomyomatosis
  5. Idiopathic
501
Q

What are the 3 causes of a dense hemithorax keeping the mediastinum central?

A
  1. Consolidation
  2. Pleural effusion
  3. Mesothelioma
502
Q

What are 4 causes of a dense hemithorax causing the mediastinum to move towards?

A
  1. Collapse
  2. Post pneumonectomy
  3. Lymphangitis carcinomatosa
  4. Pulmonary agenesis & hypoplasia
503
Q

What are 2 causes of a dense hemithorax causing the mediastinum to move away?

A
  1. Pleural effusion

2. Diaphragmatic hernia

504
Q

What are 3 causes of a white lung on CXR?

A
  1. Collapse
  2. Effusion
  3. Pneumonectomy
505
Q

What would you do for a secondary spontaneous pneumothorax (SSP)?

A
  • Admit all patients for observation +/- drain

- Oxygen

506
Q

What would you do for a primary spontaneous pneumothorax (PSP)?

A
  • Discharge if not symptomatic
  • Worsening advice, flying (radiological resolution), scuba diving (after bilateral pleurectomy), heavy lifting
  • Early review for repeat CXR
  • Smoking advice
507
Q

What 4 things should you do once the pneumothorax drain is in?

A
  1. Chest drain chart (bubbling, swinging, twisted?)
  2. Remove 24h after bubbling has stopped
  3. Usually no need for post removal CXR
  4. Surgical emphysema usually only “cosmetic”
508
Q

What 3 things should you do if the chest drain has persistent bubbling?

A
  1. Suction
  2. Larger drain
  3. Cardiothoracic surgeons
509
Q

Describe the recurrence rate of a pneumothorax?

A
  • 40% at 1 year
  • Increased in smokers
  • Elective referral for surgical (not medical) pleurodesis
510
Q

Describe the presentation of a secondary spontaneous pneumothorax (SSP)?

A
  • Can be very symptomatic with small pneumothorax

- Look carefully, if doubt about bulla vs pneumothorax consider CT

511
Q

What is a Thopaz Unit?

A

Digital Chest Drain suction

512
Q

What would you use in ambulatory management of a pneumothorax?

A

“Pleural vent” drain

513
Q

What is the normal volume of pleural fluid?

A

<15 ml

514
Q

Describe normal pleural fluid?

A

Clear, serous fluid, few cells

515
Q

Describe the diagnosis of pleural effusion?

A
  • Difficult to detect < 500ml clinically

- CXR may only show blunting of the costophrenic angle

516
Q

How does a pleural effusion present?

A

Asymptomatic or associated with SOB, cough, pleuritic chest pain or referred pain to the shoulder/abdomen

517
Q

List the 6 clinical signs of a pleural effusion?

A
  1. Reduced chest expansion
  2. Reduced tactile vocal fremitis
  3. Stony dull percussion note
  4. Quiet breath sounds
  5. Bronchial breathing above fluid level
  6. Rub with pleural inflammation
518
Q

How do pleural effusions arise?

A

When the balance between pleural fluid production & absorption has been disturbed

519
Q

List the 5 mechanisms of a pleural effusion?

A
  1. Increased hydrostatic pressure (CCF)
  2. Decreased osmotic pressure (hypoalbuminaemia)
  3. Increased vascular permeability (pneumonia)
  4. Decreased lymphatic drainage (mediastinal carcinomatosis)
  5. Increased intra-pleural negative pressure (atelectasis)
520
Q

What is a rare mechanism of pleural effusion?

A

Transdiaphragmatic passage of ascites from abdomen, chyle (chylothorax), blood (haemothorax)

521
Q

List the 5 approaches to a patient with pleural effusion?

A
  1. Clinical History
  2. Clinical features
  3. Pleural fluid analysis
  4. Further imaging
  5. Pleural biopsy
522
Q

Describe bilateral pleural effusions?

A
  • Cause usually obvious
  • Usually transudate
  • No need to sample initially
  • Treat underlying cause
523
Q

What can cardiac failure cause?

A

Unilateral effusion, particularly on the right

524
Q

What should you consider when investigating a pleural effusion?

A

Liver disease (very low protein- do not drain)

525
Q

What can chronic transudate become?

A

Exudate

526
Q

Describe unilateral pleural effusions?

A
  • Many causes (e.g. infection, malignancy, PTE, inflammatory, TB)
  • US can look for septations & suggest infection
  • Involve respiratory team early
527
Q

What are the initial investigations for a unilateral effusion?

A
  • Evidence of sepsis
  • Classical radiological appearance of empyema
  • USS characteristics
  • Needs sampling & drainage (pleural fluid pH)
528
Q

What are 5 things you would consider if the patient had a unilateral effusion & no sepsis?

A
  1. Contrast CT chest/ abdo/ pelvis
  2. Consider breast/ gynaecological malignancy
  3. Asbestos history
  4. Consider TB
  5. Liver disease
529
Q

What is pleural fluid sampling always under?

A

US guidance (real time)

530
Q

Describe the minimum pleural fluid sampling?

A
  • 100ml to cytology
  • Biochemistry for LDH/ glucose/ protein (Light’s criteria)
  • Ideally paired serum samples
  • Microbiology including TB culture, send in blood culture bottles if empyema suspected
531
Q

How should you drain pleural fluid for sampling?

A
  • Remove 1 litre if symptomatic then stop unless poor performance status
  • Do not drain to dryness
532
Q

Describe a transudate fluid?

A
  • Protein < 30 g/l
  • LDH < 2/3 upper limit of normal value for serumLDH
  • Often Bilateral
  • Usually clear
533
Q

Describe an exudate fluid?

A
  • Protein > 30 g
  • LDH > 2/3 upper limit of normal value for serum LDH
  • Pleural / serum protein ratio > 0.5
  • Pleural LDH / serum LDH ratio > 0.6
  • Usually unilateral
  • Clear, cloudy or blood-stained
534
Q

What criteria specifies an exudate fluid?

A

Light’s criteria

535
Q

What are the 4 common causes of a transudate effusion?

A
  1. Cardiac failure
  2. Hepatic cirrhosis
  3. Nephrotic syndrome
  4. Hypoalbuminaemia
536
Q

What are the 4 common causes of an exudate effusion?

A
  1. Bacterial pneumonia
  2. Malignancy
  3. Mesothelioma
  4. TB
537
Q

What is a medical thoracoscopy?

A
  • Procedure of examining the parietal pleura, visceral pleura & diaphragm with a thoracoscope
  • Rigid or semi-rigid flexible thoracoscope
538
Q

What is a Medical Thoracoscopy indicated in?

A

Undiagnosed cytology negative pleural effusions

539
Q

Describe what a medical thoracoscopy shows?

A
  • Direct visualisation of the pleural surface
  • Biopsy of areas which appear abnormal
  • Therapeutic manoeuvres e.g. complete fluid drainage & pleurodesis during the same procedure
540
Q

What is the % diagnostic rate for malignant pleural disease via medical Thoracoscopy?

A

~90%

541
Q

Describe the medical thoracoscopy procedure?

A
  • Oramorph/ atropine premed, 2-4mg midazolam
  • Patient in lateral decubitus position
  • Spot marked with ultrasound
  • Local anaesthetic (20ml 1% lidocaine)
  • Creation of pneumothorax
  • Blunt dissection, port inserted
  • Drainage of fluid with suction catheter
  • Inspection of pleural surface
  • Size 24-28 chest drain which is removed once lung re-expanded
542
Q

What is the name for a primary pleural malignancy?

A

Mesothelioma

543
Q

Describe the prognosis of mesothelioma?

A

Poor prognosis, treatment supportive

544
Q

What is a common site for metastatic spread?

A

The pleura- esp breast, ovarian, bowel, renal & lymphoma

545
Q

What would you traditionally do for a pleural malignancy?

A

Insert drain followed by medical (talc slurry) pleurodesis on ward

546
Q

What are the 5 problems with the traditional treatment of pleural malignancy?

A
  1. Poor distribution of talc- frequently fails
  2. May not come back anyway
  3. When to do in relation to chemotherapy
  4. Trapped lung
  5. High output effusion
547
Q

What are the 6 questions to ask before drainage of a pleural effusion in malignancy?

A
  1. Is the diagnosis secure?
  2. Do I need to send more samples?
  3. How symptomatic is the patient?
  4. What is the performance status?
  5. Has the patient previously felt better after drainage?
  6. Did the patient find the procedure uncomfortable before?
548
Q

What are the 4 management options for a malignancy pleural effusion?

A

1, Drain to dryness once & discharge (if diagnosis secure & already have tissue)

  1. Medical pleurodesis
  2. Thoracoscopic pleurodesis
  3. Indwelling pleural catheter (IPC)
549
Q

List the 7 patient factors for getting an indwelling pleural catheter?

A
  1. Prognosis, performance status
  2. Patient preference
  3. Symptomatic benefit from drainage
  4. Rate of accumulation
  5. Trapped lung
  6. Timing of chemotherapy
  7. Evidence
550
Q

What do upto 50% of pneumonias have?

A

Associated effusion (parapneumonic)

551
Q

Describe a complex parapneumonic effusion?

A
  • pH <7.2
  • LDH >1000
  • Glucose <2.2
  • Loculated on ultrasound
552
Q

What is an Empyema?

A

Presence of pus or bacteria

553
Q

Describe the prognosis of an Empyema?

A
  • 15% mortality
  • 15-40% require surgery
  • Median length of stay 15 days
554
Q

Describe the investigations of a pleural infection?

A
  • Initial radiology can be suggestive
  • Effusion with signs of sepsis
  • Consider if patient with pneumonia failing to improve (USS)
555
Q

How do you manage an Empyema?

A
  • Small bore chest drain (12-16F)
  • Larger drains are painful & no more effective
  • Frequent sterile saline flushes
  • IV antibiotics
  • DVT prophylaxis
556
Q

What medication would you give to manage an Empyema?

A

Fibrinolytics

  • Streptokinase
  • DNA ase & TPA (alteplase)
557
Q

What are the 3 key messages to remember for a pleural effusion?

A
  1. If bilateral treat cause & repeat imaging
  2. Do not drain at initial presentation if unilateral
  3. Discharge early
  4. Consider infection
558
Q

What are the 2 key messages to remember for a malignant pleural effusion?

A
  1. Involve respiratory - various options

2. Go by symptoms not presence of fluid

559
Q

What are the 2 key messages to remember for a pleural infection?

A
  1. Maintain index of suspicion, even if CXR non diagnostic

2. Fibrinolytics in selected cases

MBChB Year 3 (15 decks)

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