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Respiratory > Respiratory 4 > Flashcards

Respiratory 4 Flashcards

1
Q

Name a disease that is responsible for reversible airway obstruction.

A

Asthma.

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2
Q

What intrinsic factors can affect pneumonia?

A

Cold temperature, infection, stress, exercise, various pollutants.

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3
Q

What can cause acute airway obstruction?

A

Tumour or foreign bodies with distal collapse of the lung.

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4
Q

What is bronchiectasis?

A

Permanent dilation of bronchi due to obstruction and inflammation this leads to a build-up of excess mucus and predisposes someone to chest infections.

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5
Q

What is the effect of interstitial lung disease on lung volumes?

A

Reduced TCO, VC and FEV1. FEV1/FVC ratio and PEFR is normal.

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6
Q

Give an example of a chronic interstitial lung disease.

A

Interstitial pneumonia, sarcoidosis, rheumatoid.

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7
Q

What is the pathology of interstitial lung disease?

A

Increased fibrous tissue within the lung parenchyma resulting in increased stiffness and decreased expansion.

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8
Q

What is the treatment for interstitial lung disease?

A

Steroids and immunosuppressive agents. Lung transplantation may be required.

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9
Q

Why can drugs be troublesome for some people’s lungs?

A

Drugs can generate superoxide free radicals which may cause problems.

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10
Q

What is idiopathic pulmonary fibrosis?

A

Progressive fibrosis in the alveoli that limits the patients ability to respire.

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11
Q

What is the name of the lung disorder group that reflects inhaled dust/toxins?

A

Pneumoconiosis.

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12
Q

Give an example of a pneumoconiosis?

A

Coal worker’s pneumoconiosis, silicosis, asbestos exposure, extrinsic allergic alveolitis.

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13
Q

Pneumoconiosis: What is silicosis?

A

Silicosis often reflects silica exposure and may occur in grinding related occupations and mining practices.

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14
Q

What does someone with silicosis have an increased risk of developing?

A

TB.

There is a borderline increased risk of cancer.

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15
Q

Pneumoconiosis: What might be the consequences of asbestos exposure?

A
  • Lung cancer.
  • Persistent pleural effusion.
  • Diffuse pleural fibrosis.
  • Diffuse interstitial lung fibrosis.
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16
Q

What might the histological pattern of rheumatoid arthritis in association with lung disease look like?

A

Rheumatoid arthritis has a pattern paralleling usual interstitial pneumonia (UIP).

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17
Q

If the trachea, bronchi and bronchioles are involved in a disease process, is this likely to be an obstructive or a restrictive disease?

A

Obstructive.

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18
Q

If the lung parenchyma are involved in a disease process, is this likely to be an obstructive or a restrictive disease?

A

Restrictive.

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19
Q

If the chest wall is involved in a disease process, is this likely to be an obstructive or a restrictive disease?

A

Restrictive.

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20
Q

What happens to the FVC and FEV1/FVC ratio in a restrictive lung disease?

A
  • FVC reduced.

- FEV1/FVC ratio normal.

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21
Q

Give an example of a reversible obstructive lung disease.

A

Asthma.

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22
Q

What is the affect of COPD on residual volume and total lung capacity?

A

RV and TLC are increased.

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23
Q

Give an example of a restrictive lung disease.

A

Pulmonary fibrosis.

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24
Q

How would you describe the PEF for asthma.

A

Variable.

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25
Q

What factors can commonly exacerbate asthma?

A
  1. Cold weather.
  2. Exertion.
  3. Fumes.
  4. Often worse at night.
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26
Q

Name 3 diseases that might have a low transfer coefficient.

A
  1. Emphysema.
  2. Anaemia.
  3. Fibrosing alveolitis.
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27
Q

Name a disease that might have a high transfer coefficient.

A
  1. Pulmonary haemorrhage.
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28
Q

What is the name of the test that can functionally assess respiratory function?

A

6 minute walk.

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29
Q

What is consolidation on a CXR?

A

Regions of the lung filled with liquid e.g. pulmonary oedema. The areas appear white - dense.

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30
Q

What are the possible complications of bronchoscopy?

A

Pneumonia and pneumothorax.

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31
Q

Give 2 early symptoms and 2 late symptoms of lung cancer.

A
  1. Early: change in cough, wheeze, hemoptysis.

2. Later: weight loss, lethargy.

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32
Q

If a chronically breathless patient is wheezing, what is the likely cause?

A

Obstruction.

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33
Q

If a chronically breathless patient is NOT wheezing, what is the likely cause?

A

Restriction? Are there crackles on auscultation?

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34
Q

Give examples of non-respiratory causes of breathlessness.

A

Heart disease, anaemia.

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35
Q

Give 3 signs of infection.

A
  1. If the patient has a temperature.
  2. Increased neutrophils.
  3. Increased CRP.
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36
Q

What is ANCA?

A

Anti-neutrophil cytoplasmic antibody.

- Auto-immune disorder.

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37
Q

What is the mechanism of ANCA?

A

ANCA activates neutrophils and monocytes. The neutrophils adhere to endothelial cells, there is degranulation and free radicals are released. The free radicals damage the endothelium. There is further neutrophil recruitment = +ve feedback. This can result in inflammation of the vessel wall - vasculitis.

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38
Q

What disease can be caused by ANCA?

A

ANCA associated vasculitis.

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39
Q

What are common affects of rheumatoid arthritis on the lung?

A
  1. Pleural effusion.
  2. Fibrosing alveolitis.
  3. Airway disorders e.g. bronchiolitis and bronchiectasis.
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40
Q

What is Guillain Barre syndrome?

A

Demyelinating polyneuropathy.

It can present 6 weeks after flu/CMV.

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41
Q

Give 5 types of immune mediated damage.

A
  1. Tissue damage in chronic infection.
  2. Excessive immune response.
  3. Failure to control immune response.
  4. On target immune response.
  5. Off target immune response.
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42
Q

Immune mediated damage: what is the mechanism behind tissue damage in chronic infection?

A

The infection won’t clear.
There is chronic neutrophil recruitment and persistent cellular activation. Pro-inflammatory mediators are released = tissue damage.

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43
Q

Give an example of a disease where there is tissue damage due to chronic infection.

A

COPD.

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44
Q

Give examples of diseases where there is an excessive immune response.

A
  1. ARDS.

2. Asthma.

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45
Q

Give an example of a disease where there is a failure to control the immune response.

A

Alpha 1 antitrypsin disease: emphysema.

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46
Q

Give an example of a disease where there is an off target immune response.

A
  • AAV.

- Good pasteur’s syndrome.

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47
Q

Name 2 upper respiratory tract infections.

A
  1. Common cold: caused by rhinovirus.

2. Sore throat: caused by adenoviruses, EBV.

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48
Q

What viruses can cause pneumonia?

A

Adenoviruses, influenza A and B, measles, VZV.

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49
Q

What are the main antigens on influenza A?

A
  • Hemagglutinin (H).

- Neuraminidase (N).

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50
Q

What is the function of hemagglutinin?

A

‘Grappling hook’; grabs onto cells.

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51
Q

What is the function of neuraminidase?

A

‘Bolt cutters’; cuts newly formed virus loose from infected cells.

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52
Q

Which influenza pathogen is commonly behind severe and extensive outbreaks? Why?

A

Influenza A; it replicates a lot and mutations are common.

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53
Q

Define antigenic drift.

A

When there are small mutations and minor antigenic variation. Antigenic drift can cause seasonal epidemics.

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54
Q

Define antigenic shift.

A

When there are larger mutations and major antigenic variation. Antigenic shift can cause pandemics!

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55
Q

How can influenza virus be transmitted?

A
  • Aerosol: coughing and sneezing, inhale particles.

- Droplet: hand to hand.

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56
Q

What is the reproduction number?

A

The average number of secondary cases generated from a primary case.

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57
Q

Give an example of a disease with a high reproduction number.

A

Measles.

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58
Q

What is the treatment for influenza?

A

Supportive care! Antiviral medications might be used to reduce the risk of transmission.

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59
Q

Define outbreak.

A

> 2 linked cases.

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60
Q

Define epidemic.

A

More cases in a region/country.

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61
Q

Define pandemic.

A

Epidemics that span international boundaries.

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62
Q

What are the possible consequences of pandemics?

A
  1. High morbidity.
  2. Excess mortality.
  3. Social disruption.
  4. Economic disruption.
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63
Q

What factors are there to suggest that future pandemics may be likely?

A
  1. More travel.
  2. Increasing world population.
  3. Rise in intensive farming.
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64
Q

What factors are there to suggest that future pandemics may be unlikely?

A
  1. Healthier population due to medical advances.
  2. Better healthcare.
  3. Vaccination.
  4. Antivirals.
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65
Q

What can mast cell mediators affect?

A

Airways and blood vessels. They can result in bronchoconstriction and vasodilation.

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66
Q

Describe the changes in the lung 30 minutes after allergen challenge.

A

Bronchostriction.

Reduced FEV1.

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67
Q

Describe the changes in the lung 3 hours after allergen challenge.

A

Vasodilation = increased vascular permeability = inflammation.
Reduced bronchoconstriction.
Upregulated adhesion molecules.

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68
Q

Describe the changes in the lung 6 hours after allergen challenge.

A

Worsening inflammation, eosinophil involvement. 2nd wave of bronchoconstriction!

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69
Q

How would you describe the airways in asthma?

A

Hyper-reactive. This leads to inflammation.

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70
Q

What is allergic asthma?

A

When an innocuous allergen triggers an IgE mediated response. The immune recognition processes are faulty and so there is increased IgE, IL-3,4 and 5 production.

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71
Q

What is non-allergic asthma?

A

Airway obstruction induced by exercise, cold air and stress.

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72
Q

Describe the process of IgE binding to and activating mast cells.

A

IgE binds to the high affinity receptor on the mast cell surface. There is cross-linking and biochemical cascades. The mast cells are sensitised and there is degranulation.

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73
Q

What might be released on mast cell degranulation?

A
  1. Pre-formed histamine.
  2. Newly synthesised eicosanoids e.g. cysteinyl leukotrienes (cys LTs) and prostaglandin D2.
  3. Cytokines e.g. IL-3,4,5.
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74
Q

What is IL-5 responsible for?

A

Pro-inflammatory and eosinophil survival!

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75
Q

What is IL-3 responsible for?

A

Increases the number of mast cells.

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76
Q

What is IL-4 responsible for?

A

IgE synthesis.

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77
Q

Eicosanoid pathway: what enzyme converts phospholipid into arachidonic acid?

A

Phospholipase A2.

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78
Q

Eicosanoid pathway: what enzyme converts arachidonic acid into leukotrienes?

A

5 lipoxygenase.

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79
Q

Eicosanoid pathway: what enzyme converts arachidonic acid into prostaglandins?

A

Cyclooxygenase (COX).

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80
Q

Eicosanoid pathway: what protein inhibits phospholipase A2? What is the advantage of this in asthma?

A

Lipocortin inhibits phospholipase A2.
This has anti-inflammatory effects as there is reduced arachidonic acid produced and so reduced TXA2 and therefore reduced inflammation!

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81
Q

Which lung mast cell mediators are responsible for bronchoconstriction?

A

Cys-LTs and histamine.

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82
Q

Briefly describe the eicosanoid pathway.

A

Phospholipid is converted to arachidonic acid by phospholipase A2. Arachidonic acid can be converted to prostaglandins by COX or to leukotrienes by 5 lipoxygenase.

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83
Q

Which lung mast cell mediators are responsible for inflammation?

A

Cys-LTs, histamine and cytokines.

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84
Q

Which lung mast cell mediators are responsible for airway remodelling?

A

Cys-LTs, cytokines and enzymes.

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85
Q

Give 3 reasons why the airways hyper-reactive in asthmatics?

A
  1. Inflammatory infiltrate.
  2. Eosinophils.
  3. Epithelium destruction gives easier access to bronchoconstrictors.
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86
Q

What is the mechanism behind hyper-reactivity?

A

Neurogenic inflammation.

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87
Q

Describe neurogenic inflammation.

A

Sensory nerve activation initiates impulses. The impulses stimulate CGRP. CGRP is pro-inflammatory, it activates mast cells and innervates goblet cells.

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88
Q

What are the 3 main functions of CGRP in neurogenic inflammation?

A
  1. Pro-inflammatory.
  2. Mast cell activation -> mediator release.
  3. Innervation of goblet cells -> mucous release.
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89
Q

What are the 2 principles of asthma treatment?

A
  1. Alleviate symptoms.

2. Target inflammation.

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90
Q

What broad class of drugs are commonly used to alleviate symptoms?

A

Bronchodilators.

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91
Q

What broad class of drugs are commonly used to target inflammation?

A

Steroids.

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92
Q

Name 3 types of bronchodilators that are commonly used.

A
  1. Beta agonists.
  2. Muscarinic antagonists.
  3. Methylxanthines.
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93
Q

What makes LABA long acting?

A

They have increased lipophilicity.

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94
Q

What type of beta adrenergic receptors are found in the lungs?

A

Beta 2.

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95
Q

Where are beta 1 adrenergic receptors found?

A

In the heart.

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96
Q

Where are beta 3 adrenergic receptors found?

A

In adipose tissue.

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97
Q

Describe the process of PKA synthesis from beta 2 receptor activation.

A

Beta 2 interacts with Gs. This activates adenylate cyclase. Adenylate cyclase converts ATP to cyclic AMP, this then leads to PKA synthesis -> bronchodilation.

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98
Q

Give 2 functions of cAMP.

A
  1. Stabilisation of mast cells, inhibits mast cell mediator release.
  2. Relaxes airway smooth muscle.
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99
Q

What happens following activation of the M3 receptor?

A

M3 interacts with Gq. Phospholipase C is activated, this leads to DAG and IP3 production which further leads onto Ca2+ and PKC production.

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100
Q

How do muscarinic antagonists work?

A

They prevent M3 receptor activation and so there is a reduction in Ca2+ activation. This means less MLC kinase is produced and you have reduced muscle contraction.

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101
Q

How do methylxanthines work?

A

They are PDE inhibitors. They increase cAMP production and therefore PKA production. PKA inhibits MLC kinase and you have reduced muscle contraction.

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102
Q

Where is PDE4 found?

A

In the airways and inflammatory cells.

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103
Q

Which physiological process can explain how bronchodilators work?

A

Myosin light chain.

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104
Q

What is the function of MLC kinase?

A

MLC kinase phosphorylates MLC which causes muscle contraction.

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105
Q

What inhibits MLC kinase?

A

PKA.

PKA is produced from cAMP

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106
Q

What activates MLC kinase?

A

Calmodium.

Calmodium is produced from Ca2+

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107
Q

Using the myosin light chain, explain how beta agonists and methyxanthines work to alleviate symptoms.

A

Beta agonists and methylxanthines result in increased cAMP and therefor PKA. MLC kinase is inhibited and you have less smooth muscle contraction in the airway -> bronchodilation.

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108
Q

Using the myosin light chain, explain how muscarinic antagonists work to alleviate symptoms.

A

Muscarinic antagonists block M3 receptor activation and so you have a reduction in Ca2+ production. Less MLC is activated and so you have less smooth muscle contraction in the airway -> bronchodilation.

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109
Q

Where are anti-inflammatory steroids produced?

A

Adrenal cortex.

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110
Q

Where in the adrenal cortex are mineralocorticoids produced and give an example of one.

A
  • Zona glomerulosa.

- Aldosterone.

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111
Q

Where in the adrenal cortex are glucocorticoids produced and give an example of one.

A
  • Zona fasciculata.

- Hydrocortisone.

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112
Q

How do glucocorticoids work?

A

They interfere with gene transcription.

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113
Q

Give 2 effects of hydrocortisone.

A
  1. Metabolic.

2. Anti-inflammatory.

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114
Q

Give 3 potential side effects of prolonged hydrocortisone use.

A
  • Muscle wasting.
  • Osteoporosis.
  • Increased risk of infection.
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115
Q

What receptor has ‘zinc fingers’?

A

The glucocorticoid receptor.

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116
Q

What are the main cells responsible for inflammation in asthma?

A

Mast cells and eosinophils.

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117
Q

Effects of steroids: what is the effect of a positive GRE?

A

Positive GRE = increased transcription. There is also increased lipocortin production - this is anti-inflammatory as it inhibits phospholipase A2.

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118
Q

Effects of steroids: what is the effect of a negative GRE?

A

Negative GRE = suppression of cytokines.

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119
Q

Describe the mechanism behind aspirin induced asthma.

A

Aspirin inhibits COX. There is an increase in arachidonic acid. This is shunted and there is increased leukotriene production = INFLAMMATION!

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120
Q

How does anti IgE therapy work?

A

Ab binds to and neutralises free IgE; this prevents IgE binding and results in decreased mast cell sensitisation. Allergens are unable to activate mast cells.

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121
Q

What is the advantage of having inhaled medications in the management of asthma?

A

Inhaled medications are more likely to reach the target sites and there is reduced chance of side effects.

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122
Q

Name 5 groups of people who might be at increased risk on pneumonia.

A
  1. The elderly.
  2. Children.
  3. People with COPD.
  4. Immunocompromised people.
  5. Nursing home residents.
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123
Q

Describe in 3 steps the pathogenesis of pneumonia.

A
  1. Bacteria translocate to normally sterile distal airway.
  2. Resident host defence is overwhelmed.
  3. Macrophages, chemokines and neutrophils produce an inflammatory response.
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124
Q

What can cause pneumonia to be severe?

A
  1. Excessive inflammation.
  2. Lung injury.
  3. Resolution failure.
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125
Q

Describe the process of pneumonia resolution?

A

Bacteria are cleared and inflammatory cells are removed by apoptosis.

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126
Q

What protective features does the respiratory tract have against pathogens?

A

Teeth, commensal bacteria, swallowing reflex - epiglottis closes respiratory tract, mucociliary escalator, coughing and sneezing etc.

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127
Q

What symptoms might you see in someone with pneumonia?

A
  • Productive cough.
  • Sweats.
  • Fever.
  • Breathlessness.
  • Pleuritic chest pain.
  • Myalgia, headache, arthralgia suggests atypical pneumonia.
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128
Q

What signs might you see in someone with pneumonia?

A
  • Fever.
  • Signs of lung consolidation - bronchial breath sounds and dull to percuss.
  • Pleural effusion - stony dull percussion.
  • Crackles and wheeze.
  • Abnormal vital signs.
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129
Q

What investigations might you do on someone to determine whether or not they have pneumonia?

A
  • CXR - look for air bronchogram in consolidated area.
  • FBC (look at WBC’s).
  • U+E.
  • Liver function tests.
  • CRP (marker of inflammation).
  • Microbiology: sputum culture, blood culture, serology etc.
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130
Q

How can pneumonia be prevented?

A
  • Children are given PCV.
  • Smoking cessation is encouraged.
  • Influenza vaccines are given to children and the elderly.
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131
Q

What is CURB65 used for?

A

It is a way of assessing the severity of community acquired pneumonia. It predicts mortality.

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132
Q

What does CURB65 stand for?

A 
Confusion.
Urea >7mmol/L.
RR >30/min.
BP reduced - systolic <90mmHg, diastolic <60mmHg.
Age >65.
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133
Q

Why is CRB65 often used in the community?

A

Because facilities to measure urea are often not available.

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134
Q

Name 2 bacteria that are common causes of pneumonia?

A
  1. Streptococcus pneumoniae.

2. Haemophilus influenzae.

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135
Q

Describe s.pneumoniae.

A

Gram positive cocci chain. Alpha haemolytic and optochin sensitive.

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136
Q

Describe haemophilus influenzae.

A

Gram negative bacilli.

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137
Q

What antibiotic would you give to someone with haemophilus influenzae?

A

Co-amoxiclav or doxycycline.

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138
Q

What groups of people may develop pneumonia caused by klebsiella pneumoniae?

A
  • Homeless people.
  • Alcoholics.
  • People in hospital.
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139
Q

What kind of bacteria is klebsiella pneumoniae?

A

Gram negative bacilli.

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140
Q

What can be a sign of effusion on a CXR?

A

Lots of consolidation.

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141
Q

What is empyema?

A

Pockets of pus that have collected in a body cavity e.g. in the lungs.

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142
Q

Give 3 signs of empyema.

A
  1. WBC/CRP don’t settle with antibiotics.
  2. Pain on deep inspiration.
  3. Pleural collection.
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143
Q

What is the usual treatment for empyema?

A

Drainage.

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144
Q

Name 3 groups of people who might be at risk of hospital acquired pneumonia.

A
  1. Elderly.
  2. Ventilator associated.
  3. Post operative patients.
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145
Q

What is bronchiolitis?

A

Airway obstruction caused by inflammation of the bronchioles and increased mucus secretions. It is caused by RSV infection.

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146
Q

What can cause bronchiolitis?

A

Respiratory syncytial virus (RSV).

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147
Q

In what group of people is bronchiolitis common?

A

Children.

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148
Q

What is the difference between bronchitis and bronchiolitis?

A
  • Bronchiolitis: inflammation of bronchioles and increased mucus secretion due to RSV infection.
  • Bronchitis: inflammation of bronchi epithelium due to irritants and chemicals.
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149
Q

What investigations might you do in someone you suspect to have infective bronchitis?

A
  • CXR (often normal).

- Viral and bacterial swabs.

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150
Q

What is the usual cause of infective bronchitis?

A
  • Mainly viral!

- Acute bronchitis can be caused by adenoviruses.

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151
Q

Is infective bronchitis normally caused by bacterial or viral infection?

A

Viral.

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152
Q

Is pharyngitis normally caused by bacterial or viral infection?

A

Viral e.g. rhinovirus, adenovirus etc.

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153
Q

What bacteria might sometimes cause pharyngitis?

A

Streptococcus pyogenes.

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154
Q

What is the Centor criteria used for?

A

It determines the likelihood that a sore throat is bacterial.

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155
Q

What signs make up the Centor criteria?

A
  1. Tonsillar exudate.
  2. Tender/enlarged anterior cervical lymph nodes.
  3. Fever (>38°C).
  4. Absence of cough.

(3 or 4 of these = 50% chance of bacterial infection).

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156
Q

Is sinusitis usually bacterial or viral?

A

Viral.

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157
Q

What type of bacteria is Bordetella pertussis?

A

Gram negative bacilli.

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158
Q

What are the symptoms of whooping cough in adults?

A
  • Chronic cough.

- Inspiratory ‘whoop’ posttussive vomiting.

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159
Q

What agar would you culture bordetella pertussis on?

A

Bordet Gengou agar.

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160
Q

What antibiotics might you use in someone with bordetella pertussis infection?

A

Clarithromyocin.

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161
Q

When is someone vaccinated against bordatella pertussis?

A

A child is vaccinated at 8, 12 and 16 weeks and at 3 years 4 months with dTaP vaccine.

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162
Q

What causes Croup?

A

Parainfluenza virus.

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163
Q

In which group of people is Croup common?

A

Children.

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164
Q

What is croup?

A

Acute larygnotracheobronchitis - trachea, bronchi and larynx are all affected.

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165
Q

Malignant bronchial tumours can be divided into two groups; what are they?

A
  1. Non small cell cancer.

2. Small cell cancer.

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166
Q

Which type of malignant bronchial tumour fits into TNM staging?

A

Non small cell cancer.

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167
Q

Which type of malignant bronchial tumour tends to have a worse prognosis?

A

Small cell cancer.

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168
Q

Give 5 causes of lung cancer.

A
  1. SMOKING!
    - Occupational:
  2. Asbestos exposure.
  3. Radon exposure.
  4. Coal tar exposure.
  5. Chromium exposure.
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169
Q

The 5 year lung cancer survival rate is 8-10%. Why is this?

A

People often present very late with lung cancer and so treatment is much harder.

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170
Q

Give 3 main cell types that make up non small cell lung cancer?

A
  1. Squamous cell (20%).
  2. Adenocarcinoma (40%).
  3. Large cell.
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171
Q

How does PET scanning work?

A

FDG is taken up by rapidly dividing cells. Tumours therefore appear ‘hot’ on the scan. PET scans are functional rather than anatomical.

172
Q

What does TNM stand for?

A
  1. T: tumour (T1-4).
  2. N: nodal involvement (N0-3).
  3. M: metastases (M0-1).
    - Increased staging = decreased survival.
173
Q

Give 6 symptoms of local disease lung cancer.

A
  1. Chest pain.
  2. Wheeze.
  3. Breathlessness.
  4. Cough.
  5. Haemoptysis.
  6. Recurrent chest infections.
174
Q

Give 6 symptoms of lung cancer that has metastasised.

A
  1. Bone pain, especially waking up in the night from pain.
  2. Headache.
  3. Seizures.
  4. Neurological deficit.
  5. Hepatic and/or abdominal pain.
  6. Weight loss.
175
Q

Name 5 places that lung cancer might metastasise to.

A
  1. Bone.
  2. Brain.
  3. Liver.
  4. Lymph nodes.
  5. Adrenal glands.
176
Q

What are paraneoplastic syndromes?

A

Disorders triggered by immune response to a neoplasm.

177
Q

Give 5 examples of paraneoplastic syndromes.

A
  1. Finger clubbing.
  2. Anorexia.
  3. Weight loss.
  4. Hypercalcemia.
  5. Hypernatremia.
178
Q

What investigations might you do on someone to determine whether they have lung cancer?

A
  • CXR.
  • CT scan.
  • Bronchoscopy.
  • Surgical and percutaneous biopsy.
  • Bloods.
179
Q

What tests might you do on a patient to determine whether they’re fit for operation?

A
  1. ECG.
  2. Lung function tests.
  3. Determine performance status.
180
Q

It is important to ask a patient if they’ve had any previous cancers. Name 5 cancers that can spread to the lung.

A
  1. Breast.
  2. Prostate.
  3. Kidney.
  4. Melanoma.
  5. Lymphoma.
181
Q

Give an example of a malignant pleural tumour.

A

Mesothelioma.

182
Q

What can cause pleural tumours?

A

Occupational - asbestos exposure!

183
Q

Give 5 potential consequences of asbestos exposure.

A
  1. Plaques.
  2. Effusion.
  3. Asbestosis.
  4. Mesothelioma.
  5. Bronchial carcinoma.
184
Q

What are signs and symptoms of mesothelioma?

A
  1. Breathlessness.
  2. Chest pain.
  3. Weight loss.
  4. Sweating.
  5. Abdominal pain.
185
Q

What investigations might you do on someone to determine whether they have mesothelioma?

A
  • CXR.
  • CT scan.
  • Pleural biopsy.
186
Q

What is the treatment for mesothelioma?

A
  1. Symptom control.
  2. Palliative chemotherapy or radiotherapy.
  3. Radical surgery (removal of tumour blood supply).
187
Q

How does the treatment differ between local and systemic lung cancer?

A
  • Local: surgery and radiotherapy.

- Systemic: chemotherapy.

188
Q

Why is poor respiratory function in a patient you were planning to operate on a concern?

A

These patients will be at a high risk of peri-operative morbidity and mortality! There is a possibility of long term disability.

189
Q

What is the difference between radical radiotherapy and palliative radiotherapy?

A
  1. Radical: daily treatments for 4-6 weeks.

2. Palliative: the patient attends the minimum number of visits possible to control symptoms.

190
Q

Give one advantage and one disadvantage of adding chemotherapy to radiotherapy.

A
  • Advantage: survival advantage.

- Disadvantage: increased risk of toxicity.

191
Q

Give 5 side effects of radiotherapy.

A
  1. Fatigue.
  2. Anorexia.
  3. Cough.
  4. Oesophagitis.
  5. Systemic symptoms.
192
Q

What are the 3 main aims of palliative chemotherapy?

A
  1. Relieve symptoms.
  2. Improve quality of life.
  3. Shrink tumours.
193
Q

Give 4 side effects of chemotherapy.

A
  1. Alopecia.
  2. Nausea/vomiting.
  3. Peripheral neuropathy (nerve damage in extremities).
  4. Constipation or diarrhoea.
194
Q

What does pleural fluid contain?

A

Proteins e.g. albumin, globulin.

195
Q

What is the function of the pleura?

A

It allows movement of the lung and lung expansion against the chest wall.

196
Q

What produces and reabsorbs pleural fluid?

A

The parietal pleura.

197
Q

Name 3 diseases associated with the pleura.

A
  1. Pleural effusions.
  2. Pleural plaques.
  3. Pneumothorax.
198
Q

Give 5 potential causes of pleural effusion?

A
  1. Heart/renal failure (transudate).
  2. Hypoalbuminemia (transudate).
  3. Malignancy (exudate).
  4. Infection (exudate).
  5. Inflammation (exudate).
199
Q

How might you diagnose pleural effusion?

A
  1. Take a good history.
  2. Imaging.
  3. Thoracentesis - can tell you transudates v exudates.
200
Q

What is a pneumothorax?

A

Air in the pleural space which can lead to partial of complete lung collapse.

201
Q

What are the three main types of pneumothorax?

A
  1. Traumatic e.g. stab wound.
  2. Spontaneous: can be primary (PSP) or secondary (SSP).
  3. Iatrogenic.
202
Q

What is the treatment for a traumatic pneumothorax?

A

Drainage.

203
Q

Where is the chest drainage site for a pneumothorax?

A

The chest drainage site is bound by pectoralis major, latissimus dorsi and the nipple line in men or the 5th ICS in women.

204
Q

What does the medulla detect?

A

The pH (H+ conc) of the CSF.

205
Q

What do carotid and aortic bodies detect?

A

Chemoreceptors respond to increased CO2 and decreased O2.

206
Q

What is type 1 respiratory failure?

A

Hypoxia - decreased PaO2.

PaCO2 is normal or slightly low due to hyperventilation.

207
Q

What is type 2 respiratory failure?

A

Hypoxia and hypercapnia - decreased PaO2 and increased PaCO2.
There is alveolar hypoventilation.

208
Q

Give 3 signs of hypercapnia.

A
  1. Bounding pulse.
  2. Flapping tremor.
  3. Confusion.
209
Q

What can cause type 1 respiratory failure?

A
  1. Airway obstruction.
  2. Failure of O2 to diffuse into the blood.
  3. V/Q mismatch.
  4. Alveolar hypoventilation.
210
Q

What can cause type 2 respiratory failure?

A

Alveolar hypoventilation.

211
Q

Give examples of diseases that obstruct the airway and so could lead to type 1 respiratory failure.

A
  1. COPD.
  2. Obstructive sleep apnoea.
  3. Asthma.

(Can’t get O2 in but can get CO2 out).

212
Q

Name 5 things that lead to alveolar hypoventilation and so could cause type 1 and type 2 respiratory failure.

A
  1. Opiates.
  2. Emphysema.
  3. Obesity.
  4. Neuromuscular weakness e.g. MND.
  5. Chest wall deformity.
213
Q

Give examples of diseases that lead to a failure of O2 to diffuse into the blood and so could cause type 1 respiratory failure.

A
  1. Emphysema.

2. ILD e.g. IPF, sarcoidosis.

214
Q

Give examples of diseases that lead to V/Q mismatch and so could cause type 1 respiratory failure.

A
  1. Cardiac failure.
  2. PE (dead space, V/Q = ∞)
  3. Shunt (V/Q = 0)
  4. Pulmonary hypertension.
215
Q

What treatments might be given for V/Q mismatch?

A

Ventilation support e.g. CPAP and BIPAP.

216
Q

What is continuous positive airway pressure (CPAP)? When might it be used?

A

Ventilation support often given to people with OSA. It improves gaseous exchange by providing a continuous positive airway pressure.

217
Q

What is bilevel positive airway pressure (BIPAP)? When might it be used?

A

Ventilation support often given to people who have had acute exacerbations of COPD. It causes pressure to decrease when you breathe out and increase when you breathe in therefore improving ventilation to perfused alveoli.

218
Q

Name a disease that is characteristic of progressive air flow obstruction.

A

COPD.

219
Q

A young person presents to you with breathlessness, wheeze and cough. There appears to be inflammation of the airways. When you do a spirometry test the results are variable. You ask the patient to do a peak flow diary and the results of this show diurnal variation. Is the patient likely to have asthma or COPD?

A

They are likely to have asthma!
Although breathlessness, wheeze and cough are symptoms of both asthma and COPD the fact that the spirometry results are variable is a large indication that this person has asthma!
The patient is also young and COPD tends to be more common in older people.

220
Q

An older person presents to you with breathlessness, wheeze and cough. There appears to be inflammation and fibrosis of the airways and also alveolar disruption. You ask the patient to do a peak flow diary and the results of this are all abnormal. Is the patient likely to have asthma or COPD?

A

They are likely to have COPD!
Although breathlessness, wheeze and cough are symptoms of both asthma and COPD the fact that the spirometry results are consistently abnormal is a large indication that this person has COPD; in asthma there would be diurnal variation. Fibrosis and alveolar disruption are also signs of COPD and the fact that the patient is an older patient also makes COPD the more likely diagnosis.

221
Q

Secretion of which hormones might result in paraneoplastic changes?

A
  1. PTH.

2. Increased ADH (SIADH).

222
Q

Why is the prognosis for small cell lung cancer normally very poor?

A

Small cell cancers often metastasise and so prognosis is poor.

223
Q

Describe the likely presentation of someone with carcinoid tumours.

A
  1. Younger age.
  2. Characteristic neuroendocrine secreting cells.
  3. Low rates of invasion and growth.
224
Q

Are carcinoid tumours malignant?

A

Yes. Despite having low rates of invasion and growth they are still malignant.

225
Q

What is pleural fibroma?

A

Fibrous tumour of the pleura.

226
Q

What are the consequences of pleural fibroma?

A

Pleural fibromas can grow to a massive size and compress on lung tissue. Occasionally they can secrete insulin related factors and so produce hypoglycaemic symptoms.

227
Q

What is mesothelioma?

A

A high grade malignancy of the pleura that spreads around the pleural surfaces; the lung becomes encased by the tumour. It is strongly associated with asbestos exposure.

228
Q

Why is treatment of mesothelioma so difficult?

A

Mesothelioma is incurable as it is resistant to surgery, chemotherapy and radiotherapy. The average time from diagnosis to death is about 8 months.

229
Q

Briefly describe the pathogenesis of asbestosis.

A

Phagocytes are frustrated, there is chronic inflammation and permanent scarring - asbestosis!

230
Q

What are the potential consequences of occupational lung disorders?

A
  1. Increased morbidity and mortality.
  2. Loss of income.

Occupational lung disorders are avoidable and easily missed! It is important to balance health and employment and seek advice as soon as you notice any signs of lung problems.

231
Q

Describe mycobacterium tuberculosis.

A
  1. Acid fast bacilli.
  2. Has a waxy capsule.
  3. It grows slowly and therefore is hard to culture in a lab.
  4. It can resist phagolysosomal killing resulting in granulomatous disease.
232
Q

What mycobacterium can cause abdominal tuberculosis?

A

Mycobacterium bovis.

- Can be found in unpasteurised milk.

233
Q

Where are a high proportion of cases of TB found?

A

The indian sub continent e.g. India, Bangladesh, Pakistan etc.

234
Q

Give 5 risk factors for TB.

A
  1. If you live in a high prevalence area.
  2. IVDU.
  3. Homeless.
  4. Alcoholic.
  5. HIV+.
235
Q

How is TB transmitted?

A

Aerosol transmission - mycobacterium TB bacilli are inhaled and enter the lung.

236
Q

Describe pulmonary infection of TB.

A

Bacilli settle in lung apex. Macrophages and lymphocytes mount an effective immune response that encapsulates and contains the organism forever.

237
Q

Describe the pathogenesis of pulmonary TB disease.

A
  1. Bacilli and macrophages form primary focus.
  2. Mediastinal lymph nodes enlarge.
  3. Primary focus and enlarged lymph nodes = primary complex.
  4. Granuloma develops into a cavity.
  5. The cavity is filled with TB bacilli - these are expelled when the patient coughs.
238
Q

TB disease: Where in the lung is a granuloma cavity most likely to develop?

A

Most likely to develop in the apex of the lung as there is more air and less blood supply/immune cells.

239
Q

Presentation of TB: what systemic symptoms might you see?

A
  1. Weight loss.
  2. Night sweats.
  3. Anorexia.
  4. Malaise.
240
Q

Presentation of TB: what pulmonary TB symptoms might you see?

A
  1. Cough.
  2. Chest pain.
  3. Breathlessness.
  4. Haemoptysis.
241
Q

What might you see on a CXR taken from someone with TB?

A
  1. Consolidation.
  2. Collapse.
  3. Pleural effusion.
242
Q

Name 6 places where TB might spread to?

A
  1. Bone and joints - pain and swelling.
  2. Lymph nodes - swelling and discharge.
  3. CNS - TB meningitis.
  4. Miliary TB - disseminated.
  5. Abdominal TB - ascites, malabsorption.
  6. GU TB - sterile pyuria, WBC in GU tract.
243
Q

What test might you do to diagnose latent TB?

A

Mantoux test - stimulates type 4 hypersensitivity reaction.

244
Q

What drugs are given in the treatment of TB?

A

Rifampicin (6 months).
Isoniazid (6 months).
Pyrazinamide (2 months).
Ethambutol (2 months).

245
Q

TB treatment: which 2 drugs are taken for the entire 6 months?

A
  1. Rifampicin.

2. Isoniazid.

246
Q

TB treatment: which 2 drugs are taken for only the first 2 months?

A
  1. Pyrazinamide.

2. Ethambutol.

247
Q

TB treatment: How long do you take Rifampicin for?

A

6 months.

248
Q

TB treatment: How long do you take Isoniazid for?

A

6 months.

249
Q

TB treatment: How long do you take Pyrazinamide for?

A

2 months.

250
Q

TB treatment: How long do you take Ethambutol for?

A

2 months.

251
Q

Give 3 potential side effects of Rifampicin.

A
  1. Red urine.
  2. Hepatitis.
  3. Drug interactions; rifampicin is an enzyme inducer.
252
Q

Give 2 potential side effects of Isoniazid.

A
  1. Hepatitis.

2. Neuropathy.

253
Q

Give 3 potential side effects of Pyrazinamide.

A
  1. Hepatitis.
  2. Gout.
  3. Rash.
254
Q

Give 1 potential side effect of Ethambutol.

A
  1. Optic neuritis.
255
Q

Compliance in taking TB medication is critical. Why?

A

Resistance and relapse may be likely if the patient is non-compliant.

256
Q

Why does TB treatment need to last for 6 months?

A

TB treatment lasts for at least 6 months to ensure all the dormant bacteria have ‘woken up’ and been killed.

257
Q

What is the acronym commonly used for the drugs taken in TB treatment?

A 
HRZE.
HR = 6 months. 
ZE = 2 months.
- H - isoniazid. 
- R - rifampicin.
- Z - pyrazinamide.
- E - ethambutol.
258
Q

TB treatment: Give 4 factors that can increase the risk of drug resistance?

A
  1. If the patient has had previous treatment.
  2. If they live in a high risk area.
  3. If they have contact with resistant TB.
  4. If they have a poor response to therapy.
259
Q

What are the problems associated with drug resistance in TB treatment?

A
  1. TB becomes more difficult to treat.
  2. Medication course > 20 months.
  3. Increased risk of side effects.
  4. Increased relapse rate.
260
Q

How can TB be prevented?

A
  1. Active case finding - reduce infectivity.
  2. Detect and treat latent TB.
  3. Vaccination - BCG.
261
Q

What are interstitial lung diseases?

A

Diseases of the alveolar/capillary interaction. There is often scarring around the alveoli and so an increased diffusion pathway for gaseous exchange.

262
Q

What are the 5 major categories of interstitial lung disease?

A
  1. Associated with systemic diseases e.g. rheumatological.
  2. Environmental aetiology e.g. fungal, dusts.
  3. Granulomatous disease e.g. sarcoidosis.
  4. Idiopathic e.g. IPF.
  5. Other.
263
Q

Give 4 major signs and symptoms of interstitial lung disease.

A
  1. Cough.
  2. Breathlessness.
  3. Finger clubbing.
  4. Evidence of systemic disease.
264
Q

Would pulmonary function tests taken from someone with interstitial lung disease show a restrictive or obstructive pattern?

A

They would be restrictive!

There is decreased gas transfer and a reduction in PaO2.

265
Q

Who does idiopathic pulmonary fibrosis usually effect?

A

It tends to be a disease of the elderly.

266
Q

Give 3 signs/symptoms of IPF.

A
  1. Dyspnoea on exertion.
  2. Dry cough.
  3. Elderly effected.
267
Q

What is IPF?

A

A disease characterised by chronic inflammation and permanent scarring in the alveoli. Respiratory ability is affected. Chest infection and hypoxic damage are likely.

268
Q

Give 4 risk factors for IPF.

A
  1. Smoking.
  2. Dust exposure.
  3. Exposure to infectious agents.
  4. Long term antidepressant use.
269
Q

What treatment is used in IPF?

A
  • Lung transplant and supportive care is the only treatment shown to increase survival.
  • If the patient has an acute exacerbation, broad spectrum antibiotics may be used.
270
Q

What is the general treatment for all interstitial lung disease?

A
  1. Remove the exposure!

2. Steroids.

271
Q

What kind of disease is sarcoidosis?

A

It is a granulomatous disease!

It can affect any organ system but typically affects the lungs/lymph nodes.

272
Q

Is sarcoidosis a restrictive or obstructive disease?

A

Pulmonary function tests would show restrictive patterns.

273
Q

What is the usual treatment for sarcoidosis?

A

Steroids.

274
Q

Define bronchiectasis.

A

Irreversible and abnormal dilation of the bronchi with chronic inflammatory and fibrotic changes.

275
Q

Describe the pathogenesis of bronchiectasis.

A

Failed mucocilliary clearance and impaired immune function mean that a microbe can easily invade and cause infection. This leads to inflammation and therefore progressive lung damage. Bronchitis -> bronchiectasis -> fibrosis.

276
Q

What can cause bronchiectasis?

A
  1. Often post-infective e.g. previous pneumonia, TB or whooping cough infection.
  2. Congenital causes e.g. primary ciliary dyskinesia.
  3. 50% idiopathic.
277
Q

Which bacteria might cause bronchiectasis?

A
  1. Haemophilus influenzae.
  2. Pseudomonas aeruginosa.
  3. Staphylococcus aureus.
278
Q

Give 6 symptoms of bronchiectasis.

A
  1. Chronic productive cough.
  2. Recurrent chest infections.
  3. Dyspnoea and wheeze.
  4. Recurrent exacerbations.
  5. Chest pain.
  6. Haemoptysis.
279
Q

What investigations might you do on someone to determine whether they have bronchiectasis?

A
  • High resolution CT scan.
  • Spirometry - would be obstructive.
  • Sputum culture.
  • CXR.
280
Q

What is the treatment/management for bronchiectasis?

A
  1. Education.
  2. Smoking cessation.
  3. Annual influenza and pneumococcal vaccinations.
  4. Antibiotics.
  5. Anti-inflammatories.
  6. Bronchodilators.
  7. Improved mucus clearance e.g. physiotherapy.
281
Q

Describe the pathogenesis of cystic fibrosis.

A

There is a defect in chromosome 7 coding CFTR protein. Cl- transport is affected and there is production of thickened mucus secretions.

282
Q

How is cystic fibrosis passed on?

A

It is an autosomal recessive condition.

1 in 25 people are carriers.

283
Q

A common mutation in which gene can cause CF?

A

A mutation in ∆F508.

284
Q

Give 6 potential complications of CF.

A
  1. Malnutrition due to malabsorption.
  2. Respiratory failure and cor pulmonale.
  3. Weight loss and growth retardation.
  4. Infertility, very common in males due to defect in vas deferens.
  5. Nasal polyps.
  6. Diabetes mellitus due to pancreatic insufficiency.
  7. Delayed puberty.
  8. Sinusitis.
  9. Breathlessness
  10. Finger clubbing.
  11. Frequent respiratory infections (-> bronchiectasis).
  12. Salty sweat
285
Q

What is the management of CF?

A
  1. Prevention e.g. vaccination.
  2. Segregation to prevent spread.
  3. Surveillance - monitor FEV1.
  4. Enzyme supplements for pancreatic insufficiency.
  5. Anti-pseudomonal antibiotic therapy.
  6. Physical therapies e.g. airway clearance and exercise.
  7. Supporting therapies e.g. ensure a good diet.
286
Q

Define pulmonary hypertension.

A
  • mPAP > 25mmHg.

- Secondary RV failure.

287
Q

What can cause an increase in mPAP?

A

Increased resistance to flow.

Increased flow rate.

288
Q

Give 5 causes of pulmonary hypertension.

A
  1. Hereditary.
  2. Idiopathic.
  3. Drug use.
  4. HIV infection.
  5. Pulmonary hypertension secondary to left heart disease (valvular, systolic/diastolic dysfunction).
289
Q

Give 5 symptoms of pulmonary hypertension.

A 
Initial symptoms:
1. Dyspnoea on exertion. 
2. Lethargy.
3. Fatigue.
4. Syncope.
Symptoms as RV failure develops:
1. Pulmonary oedema.
2. Abdominal pain.
290
Q

What investigations might you do in someone to determine whether they have pulmonary hypertension?

A
  1. ECG - see if there’s RV hypertrophy.
  2. Spirometry.
  3. CXR - enlarged proximal pulmonary arteries.
  4. Echocardiography.
291
Q

What might you notice in the ECG take from someone with pulmonary hypertension?

A

There might be signs of RV hypertrophy.

292
Q

What might you notice in a CXR take from someone with pulmonary hypertension?

A

There might be enlarged proximal pulmonary arteries which taper distally.

293
Q

Describe the usual treatment for someone with pulmonary hypertension.

A
  1. Initial treatment is O2.
  2. Warfarin (due to risk of thrombosis).
  3. Diuretics (for oedema).
  4. Ca2+ blockers (pulmonary vasodilators).
  5. Treat underlying cause.
294
Q

Why might someone with pulmonary hypertension experience peripheral oedema?

A

Blood accumulates in the pulmonary artery. The RV experiences a greater afterload and works harder to get blood out of the ventricle and into the pulmonary artery. There is RV hypertrophy and right heart failure. This results in peripheral oedema.

295
Q

Pulmonary embolism: where might an emboli arise from?

A

Emboli often arise from a dislodged DVT - from iliofemoral veins.

296
Q

What is the consequence of a small, peripheral PE?

A

Infarction!

There is ventilation but no perfusion; dead space.

297
Q

What is the consequence of a large, central PE?

A

Ischaemia!

There is resistance to flow which can also result in RHF.

298
Q

What are symptoms of a small, peripheral PE?

A
  • Breathlessness.

- Pleuritic chest pain.

299
Q

What are symptoms of a large, central PE?

A
  • Severe central chest pain.

- Pale and sweaty.

300
Q

What investigations might you do in someone to determine whether they have PE?

A
  • CXR.
  • ECG.
  • D-dimer.
  • V/Q lung scan - shows ventilated areas with perfusion defects.
  • CTPA - can detect emboli.
301
Q

What is D dimer?

A

A small protein fragment found after a blood clot is degraded by fibrinolysis.

302
Q

The Wells scoring system is used to work out the probability of a person having a PE. Name 5 factors that the scoring system uses.

A
  1. Clinical signs/symptoms of DVT.
  2. HR > 100bpm.
  3. Recent immobilisation.
  4. Previous DVT/PE.
  5. Haemoptysis.
  6. Malignancy.
    Score >4 - PE likely.
303
Q

Describe the treatment for PE.

A
  1. Thrombolysis is used for a large PE.
  2. LMWH (anti-coagulant) and oral warfarin.
  3. NOAC (anticoagulant).
  4. Analgesia for pain relief.
304
Q

What diseases might be in the differential diagnosis of PE?

A
  1. Asthma.
  2. COPD.
  3. Pneumonia.
  4. MI.
305
Q

What is pulmonary vasculitis?

A

Inflammation of the pulmonary arterial wall.

306
Q

Why are immunosuppressants given as treatment to people with pulmonary vasculitis?

A

Pulmonary vasculitis is autoimmune associated.

307
Q

What 2 categories can asthma be divided into?

A
  1. Allergic asthma (extrinsic); atopic. IgE and mast cell involvement.
  2. Non allergic asthma (intrinsic).
308
Q

Describe asthma.

A

An inflammatory disease characterized by hyper-responsive airways. Airway obstruction is reversible. There is inappropriate smooth muscle contraction.

309
Q

Extrinsic asthma: what happens when IgE binds to mast cells?

A

Vasoactive substances are released causing bronchoconstriction, oedema, bronchial inflammation and mucus hyper-secretion.

310
Q

Name 5 factors that can exacerbate asthma.

A
  1. Allergens.
  2. Viral infections.
  3. Cold air.
  4. Exercise.
  5. Stress.
  6. Cigarette smoke.
  7. Drugs e.g. aspirin.
311
Q

What occupations may be associated with an increased risk of developing asthma?

A
  1. Paint sprayers - exposure to fumes.
  2. Animal breeders.
  3. Bakers.
  4. Laundry workers.
312
Q

What are the symptoms of asthma?

A
  1. Breathlessness.
  2. Diurnal variation - often worse in the morning.
  3. Cough.
  4. Episodic wheeze.
  5. Chest tightness.
313
Q

What investigations might you do on someone to determine whether they have asthma?

A
  1. PEFR.
  2. Spirometry should show an obstructive pattern; FEV1 < 80%, FEV1/FVC < 0.7, PEFR - variable.
  3. Test for atopy; RAST, skin prick test.
  4. CXR.
  5. Eosinophil count.
  6. O2 saturation.
314
Q

How can reversibility be tested in asthma?

A

When given a beta agonist there will be a 400ml increases in FEV1 OR a 20% improvement in PEFR.

315
Q

What tool can be used to assess the severity of asthma?

A

RCP3

  • Recent nocturnal waking?
  • Usual asthma symptoms during the day?
  • Interference with ADL’s?

May also want to ask about whether the patient has used any rescue medications.

316
Q

What is the function of RCP3?

A

It is used to assess the severity of asthma.

317
Q

Describe the management/treatment of asthma.

A
  • Improve control and avoid triggers!
  • Smoking cessation is important.
  • Beta agonists provide symptomatic relief.
  • ICS are anti-inflammatory.
  • Sometimes a short course of systemic steroids might be used.
318
Q

Give 5 side effects of systemic steroids.

A
  1. Diabetes.
  2. Osteoporosis.
  3. Hypertension.
  4. Oral candida (oral steroids).
  5. Skin thinning.
319
Q

What 4 measurements can be used to diagnose acute severe asthma?

A
  1. RR > 25.
  2. HR > 110.
  3. PEFR 35-50% predicted.
  4. Unable to complete a sentence in one breath.
320
Q

What is the first line treatment for acute severe asthma?

A

Nebulised salbutamol with oxygen.

IV corticosteorids and abx if evidence of infection.

321
Q

Respiratory immunity: describe the innate immune response.

A

Mucous, mucociliary escalator, macrophages and neutrophils all play a role in the innate immune response. Cough reflex and epiglottis closing off trachea on swallowing.

322
Q

Respiratory immunity: describe the adaptive immune response.

A
  • B cells produce mainly IgG and IgA antibodies.

- T cells - CD4, CD8 and regulatory.

323
Q

How can neutrophils destroy bacteria?

A

Neutrophil bactericidal functions include ROS, proteases and NETs.

324
Q

What can affect the cough reflex?

A
  • Pain.
  • Sedation.
  • Opiates.
325
Q

What can affect cilia function?

A
  • Infection.

- Primary dyskinesia.

326
Q

What are the 3 types of immunosuppression?

A
  1. Granulocyte defect - associated with chemotherapy.
  2. B cell defect - associated with rituximab and hematological malignancy.
  3. T cell defect - associated with immunosuppression/HIV.

All result in an increased risk of infection.

327
Q

What is a granulocyte defect associated with?

A

Chemotherapy.

328
Q

What is a T cell defect associated with?

A

Immunosuppression and HIV.

329
Q

What is a B cell defect associated with?

A

Rituximab and hematological malignancy. There is an increased risk of encapsulated bacteria infection e.g. H.influenzae.

330
Q

Define neutropenia.

A

A disease characterised by having an abnormally low concentration of neutrophils in the blood.

331
Q

What can cause neutropenia?

A

Often iatrogenic causes e.g. chemotherapy.

332
Q

Give 4 examples of iatrogenic suppression.

A
  1. Corticosteroid use.
  2. Chemotherapy.
  3. Immune suppression after organ transplant.
  4. Rituximab.
333
Q

Give 4 examples of non-specific immunosuppression.

A
  1. Malnutrition.
  2. Alcohol.
  3. Sepsis.
  4. Trauma.
334
Q

How can illness be prevented in the immunocompromised?

A
  1. Hand hygiene.
  2. Education e.g. avoid live vaccines.
  3. Isolation.
  4. Screen for TB before anti TNF therapy.
  5. PCP prophylaxis of < CD4 count.
335
Q

Describe the usual presentation of pulmonary infection in the immunocompromised?

A
  1. Pyrexia.
  2. Lethargy.
  3. Cough.
  4. Breathlessness.
  5. Hypoxic.
336
Q

An immunocompromised person presents with a rapid onset pulmonary infection. Is this likely to have a bacterial or viral cause?

A

Rapid onset is likely to be bacterial.

337
Q

An immunocompromised person presents with a slow onset pulmonary infection. Is this likely to have a bacterial or viral cause?

A

Slow onset is likely to be CMV, aspergillus or cryptococcus.

338
Q

Describe the signs and symptoms of PCP.

A
  • Progressive breathlessness and dry cough.
  • Lymphopenia typical (CD4<200).
  • Hypoxia.
339
Q

What is the usual treatment for PCP?

A

High dose co-trimoxazole.

Consider secondary prophylaxis.

340
Q

Who might be at risk of CMV?

A

Transplant recipients or HIV patients.

341
Q

Why is treatment of CMV difficult?

A

Treatment is difficult due to long duration and potential toxicity.

342
Q

Define CF.

A

An autosomal recessive disease resulting in abnormal exocrine gland function.

343
Q

The airways in a person with bronchiectasis often become chronically colonised. What is the airway of a neonate likely to be colonised with?

A

s.aureus.

344
Q

The airways in a person with bronchiectasis often become chronically colonised. What is the airway of a child likely to be colonised with?

A

h.influenzae.

345
Q

The airways in a person with bronchiectasis often become chronically colonised. What is the airway of an adult likely to be colonised with?

A

pseudomonas aeruginosa.

346
Q

Name 3 less common ‘atypical’ pathogens that can be responsible for causing pneumonia.

A
  1. Mycoplasma pneumoniae.
  2. Chlamydia psittaci/pneumoniae.
  3. Coxiella burnetti.
  4. Legionella pneumophilia.
347
Q

How can less common ‘atypical’ pathogens responsible for causing pneumonia be identified?

A

They are hard to grow in culture and so serology and antigen tests are often used.

348
Q

What antibiotic might be used against less common ‘atypical’ pathogens responsible for causing pneumonia?

A

Macrolides like clarithromyocin as they are often resistant to beta lactams.

349
Q

A special culture medium is needed to grow TB. What is the medium called?

A

Lowenstein Jensen Slope.

350
Q

Lowenstein Jensen Slope is a medium used to grow TB. What is special about this medium?

A
  1. It contains growth factors that promote mycobacterial growth.
  2. It contains small amounts of penicillin that prevent pyogenic bacteria growth.
351
Q

What might a lymph node biopsy from someone with TB show?

A

Caseating granuloma.

352
Q

Name a disease that causes a reduction in TLCO.

A

Asthma.

353
Q

What is TLCO?

A

The extent to which O2 passes from the alveoli into the blood.

354
Q

What 3 factors can affect TLCO?

A
  1. Alveoli/capillary interaction.
  2. Hb concentration.
  3. Cardiac output.
355
Q

How long is the treatment for an idiopathic pulmonary embolism?

A

At least 6 months.

356
Q

How much fluid is contained within the healthy pleural space?

A

15ml.

357
Q

Which chromosome codes or CFTR?

A

Chromosome 7.

358
Q

Name 2 ions that CFTR transports.

A
  1. Chloride.

2. Thiocynate.

359
Q

Give 3 radiological indications for bronchoscopy.

A
  1. Lobar collapse.
  2. Presence of a mass.
  3. Persistent consolidation.
360
Q

Give 3 non-radiological indications for bronchoscopy.

A
  1. Hemoptysis.
  2. Cough.
  3. Wheeze.
  4. Stridor.
361
Q

What percentage of asthma is thought to be caused by occupational factors?

A

10%.

362
Q

What type of T lymphocyte is involved in asthma?

A

CD4+.

363
Q

What are the 3 characteristic features of asthma?

A
  1. Airflow obstruction.
  2. Hyper-responsive airways to a range of stimuli.
  3. Bronchial inflammation.
364
Q

Define atopy.

A

The tendency to develop IgE mediated responses to common aeroallergens.

365
Q

Describe the process of airway remodelling in asthma.

A
  1. Hypertrophy and hyperplasia of smooth muscle cells narrow the airway lumen.
  2. Deposition of collagen below the BM thicken the airway wall.
  3. Eosinophils also play a role in remodelling.
366
Q

Give 3 histo-pathological changes that occur in asthma.

A
  1. Basement membrane thickening.
  2. Epithelium metaplasia; increased no. of goblet cells leads to mucus hypersecretion.
  3. Increase in inflammatory gene expression on many cell types.
367
Q

What are the signs of asthma?

A
  1. Secretions.
  2. Obstructive spirometry.
  3. Variable PEFR.
  4. Reversibility when given beta-2-agonist, FEV1 > 20%.
  5. Diurnal variation.
368
Q

What is hypersensitivity pneumonitis (EAA)?

A

Inhalation of organic dusts leads to a type 3 hypersensitivity reaction; there is an inflammatory response in the alveoli and small airways.

369
Q

Name a cause of hypersensitivity pneumonitis (EAA).

A
  1. Farmer’s lung; due to mouldy hay and aspergillus spores.

2. Bird fancier’s lung; due to proteins present in bird faeces.

370
Q

What can happen if exposure is persistent in someone with farmer’s lung?

A

Progressive fibrosis can occur. There may be signs of weight loss, dyspnoea and cough too.

371
Q

Give 3 symptoms of hypersensitivity pneumonitis (EAA).

A
  1. Fever.
  2. Malaise.
  3. Cough.
372
Q

What are occupational lung disorders?

A

Lung disorders due to a response to inhaling something at work e.g. fumes, dust, gas, aerosol.

373
Q

Give 5 damage mechanisms of occupational lung disorders.

A
  1. Direct injury.
  2. Infection.
  3. Allergy e.g. EAA.
  4. Chronic inflammation e.g. COPD.
  5. Destruction of lung tissue e.g. emphysema.
  6. Lung fibrosis.
  7. Carcinogenesis.
374
Q

Give 4 ways in which occupational lung disorders can be prevented.

A
  1. Risk assessment.
  2. Legal requirement under COSHH.
  3. Prevent and minimise exposure to harmful substances.
  4. Monitor worker’s health so health problems can be identified early.
375
Q

Give an example of an occupational asthma.

A

Baker’s asthma; flour being the harmful allergen.

376
Q

How might you diagnose someone with having occupational asthma?

A
  1. Do a PEFR test at their place at work and take a history to determine whether their symptoms are worse at work.
  2. Serum immunology looking for IgE to a particular workplace allergen.
377
Q

Bronchiectasis is a disease characterised by irreversible dilation of the bronchi. True or False: spirometry shows an obstruction pattern.

A

True!
Even though bronchi are dilated there is chronic inflammation, scarring and thickening of the bronchi wall which result in airway obstruction.

378
Q

Give 5 signs of sarcoidosis.

A
  1. Bi-lateral hilar lymphadeonopathy (BHL).
  2. Erythema nodosum.
  3. Uveitis.
  4. Non productive cough, SOB, wheeze.
  5. Metabolic affect of sarcoidosis = hyperacalcaemia -> nephrocalcinosis.
  6. Arthalgia.
  7. Hepatosplenomegaly.
  8. Neurological: inflammation of the meninges and seizures.
  9. Heart block.
  10. Lung fibrosis.
  11. Finger clubbing is rare!
379
Q

Give 5 signs of pulmonary hypertension.

A
  1. RV hypertrophy (ECG).
  2. Loud pulmonary secondary sound.
  3. Right parasternal heave.
  4. Enlarged proximal pulmonary arteries (CXR).
  5. In advanced disease there are signs of RHF, elevated JVP, hepatomegaly and pleural effusion etc.
380
Q

What is Wegener’s granulomatosis?

A

Vasculitis of unknown aetiology. It commonly involves the upper airway and endo-bronchi.

381
Q

What are the symptoms of wegener’s granulomatosis?

A
  1. Rhinorrhoea.
  2. Nasal mucosa ulceration.
  3. Cough.
  4. Haemoptysis.
  5. Pleuritic chest pain.
382
Q

What would serum tests for someone with Wegener’s granulomatosis show?

A
  • C-ANCA and anti-PR3 positive.
383
Q

How would you treat a pleural effusion with a transudate cause e.g. heart/renal failure?

A

You would treat the underlying cause e.g. the heart failure.

384
Q

What are the symptoms of wegener’s granulomatosis?

A
  1. Rhinorrhoea.
  2. Nasal mucosa ulceration.
  3. Cough.
  4. Haemoptysis.
  5. Pleuritic chest pain.
385
Q

What would serum tests for someone with Wegener’s granulomatosis show?

A
  • C-ANCA and anti-PR3 positive.
386
Q

How would you treat a pleural effusion with a transudate cause e.g. heart/renal failure?

A

You would treat the underlying cause e.g. the heart failure.

387
Q

How would you treat a pleural effusion with an exudate cause e.g. inflammation?

A

Drainage.

388
Q

What is the function of inositol trisphosphate?

A

Inositol trisphosphate (IP3) increases free cytosolic Ca2+ by releasing Ca2+ from intracellular compartments. Ca2+ activates MLC kinase = bronchial smooth muscle contraction.

389
Q

What does activation of the M3 receptor cause?

A
  1. Bronchoconstriction.
  2. Vasodilation.
  3. Glandular secretions.
390
Q

What is the treatment for someone with mild pneumonia (a CURB65 score of 0-1)?

A

PO amoxicillin.

391
Q

Where should someone with mild pneumonia (a CURB65 score of 0-1) be treated?

A

In the community.

392
Q

What is the treatment for someone with moderate pneumonia (a CURB65 score of 2)?

A

PO amoxicillin and clarithromyocin.

393
Q

Where should someone with moderate pneumonia (a CURB65 score of 2) be treated?

A

In hospital.

394
Q

What is the treatment for someone with severe pneumonia (a CURB65 score of >3)?

A

IV co-amoxiclav and clarithromyocin.

395
Q

Where should someone with severe pneumonia (a CURB65 score of 3) be treated?

A

In hospital.

396
Q

Where should someone with severe pneumonia (a CURB65 score of >4) be treated?

A

In hospital, consider admission to critical care.

397
Q

A 66 y/o patient presents to you with fever and a productive cough. On examination you notice they are their confused. Their vital signs are: RR - 35; BP - 80/55 and HR: 130. You measure their urea and it comes back at 8mmol/L.

a) What is this patients CURB65 score?
b) Where should they be treated?
c) Describe the treatment for this patient.

A

a) Their CURB65 score is 5.
b) This patient should be treated in hospital and admitted to critical care.
c) The patient should be given IV clarithromyocin and co-amoxiclav.

398
Q

Give 2 potential complications of pneumonia.

A
  1. Empyema.

2. Lung abscess.

399
Q

Describe the pathophysiology of a tension pneumothorax.

A

A pleural tear creates a 1-way valve through which air passes in inspiration -> increased intra-pleural pressure -> respiratory distress, shock and cardiac rest.

400
Q

What is the treatment for a tension pneumothorax?

A

Immediate needle decompression.

401
Q

Give 5 risk factors for PE.

A
  1. Obesity.
  2. Recent surgery.
  3. Malignancy.
  4. Immobility.
  5. OCP/HRT.
402
Q

When looking to diagnose IPF, what 3 findings would you look for on pulmonary function tests?

A
  1. Reduced TLCO.
  2. Restrictive spiromerty: low FEV1 and FVC but normal ratio.
  3. Low/normal PaO2.
403
Q

In what two types of interstitial lung disease will neutrophil levels be raised?

A

IPF and DIP.

404
Q

A patient presents with breathlessness. On examination they have absent breath sounds and their chest produces a stony dull sound on percussion. They have a PMH of heart failure. What is the likely cause of their symptoms?

A

Pleural effusion.

405
Q

Give 3 pulmonary symptoms of sarcoidosis.

A
  • Cough.
  • SOB.
  • Wheeze.
406
Q

What is the effect of sarcoidosis on the skin?

A

Erythema nodosum.

407
Q

What is the effect of sarcoidosis on the eyes?

A

Uveitis.

408
Q

Give a metabolic effect of sarcoidosis.

A

Hypercalcaemia.

409
Q

What is the effect of sarcoidosis on bone?

A

Arthralgia.

410
Q

What is the effect of sarcoidosis on the liver?

A

Hepatosplenomegaly.

411
Q

Give a neurological effect of sarcoidosis.

A
  • Inflammation of the meninges.

- Seizures.

412
Q

Give 2 diseases that might be in the differential diagnosis of sarcoidosis.

A
  1. Lymphoma.

2. Pulmonary TB.

413
Q

A lady who has recently had pneumonia presents to you with SOB and chronic cough. She is producing copious amounts of purulent sputum. What is the likely diagnosis?

A

Bronchiectasis.

414
Q

Give 4 signs of a large PE.

A
  1. Shocked.
  2. Central cyanosis.
  3. Raised JVP.
  4. Accentuation of second heart sound.
415
Q

Infection with a gram negative bacteria is a particular concern in patients with CF. What is this organism and how can infection be prevented?

A
  • Pseudomonas Aeruginosa.

- Nebulised anti-pseudomonal antibiotic therapy and regular sputum cultures.

416
Q

A patient comes in with bilateral lymphadenopathy. Give 3 conditions that you would include in your differential diagnosis?

A
  1. Local infection e.g. tonsilitis/TB.
  2. Lymphoma.
  3. Sarcoidosis.
417
Q

Why does TB cause hypercalcaemia?

A

Granulomatous diseases -> increased vitamin D production and so increased bone resorption, increased absorption from gut and increased re-absorption from kidney.

This is also seen in sarcoidosis.

418
Q

What syndrome may result from an apical lung cancer affecting the T1 nerve root?

A

Horner’s syndrome.

419
Q

Give 5 signs of Horner’s syndrome.

A
  1. Anhydrosis.
  2. Miosis - pupil constriction.
  3. Ptosis.
  4. Loss of ciliospinal reflex.
  5. Enophthalmos - backwards displacement of the eyeball.
420
Q

Is TLC increased or decreased in restrictive lung diseases?

A

TLC is decreased.

421
Q

State the name of the pathological lesion that characterises primary tuberculosis?

A

Ghon complex.

422
Q

State two socioeconomic factors that are associated with an increased prevalence of tuberculosis.

A
  1. Overcrowding.
  2. Poverty.
  3. Lower socio-economic class.
423
Q

State why cystic fibrosis increases the viscosity and tenacity of the bronchial mucus?

A

Failure to excrete Cl- leads to Na+ retention. This then leads to H2O retention.

424
Q

Which type of NSCC is most common in smokers?

A

Squamous cell carcinoma.

425
Q

From what cells are SCC derived from and what is the significance of this?

A

Neuroendocrine cells.

Can secrete peptide hormones such as ACTH, PTHrP, ADH and HCG.

426
Q

A man with squamous cell carcinoma complains of a dull ache in his back, being very thirsty, and tired. What is the cause of these symptoms?

A

Squamous cell carcinomas can release PTHrP.

Respiratory (9 decks)

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