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Cardiorespiratory > Respiratory > Flashcards

Respiratory Flashcards

1
Q

What is a defining feature of asthma?

A

Expiration wheeze

Reversible air flow limitation - usually with a bronchodilator

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2
Q

What are the possible classifications of an asthma diagnosis?

A
  1. Possible
  2. Probable
  3. Definite
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3
Q

What immune profile suggests atopy?

A

Th2

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4
Q

Which immune profile strengthens the case for the hygiene hypothesis?

A

Th1 vs Th2

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5
Q

Which immune cells are seen in asthma?

A

Eosinophils
CD4+ T lymphocytes
Mast cells
Neutrophils (especially in severe asthma)

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6
Q

Which immune cells are particularly seen in severe asthma?

A

Neutrophils

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7
Q

What histological features are seen in asthma?

A

Thickened basement membrane
New vessel formation
Epithelial disruption
Mucus gland hypertrophy

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8
Q

Which conditions can result in airflow obstruction?

A 
COPD
Bronchiectstasis
Inhaled foreign body
Obliterative bronchiolitis
Large airway stenosis
Lung cancer
Sarcoidosis
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9
Q

How can airflow obstruction be tested for?

A

Reversibility testing

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10
Q

Which test is no use if there is no suspected airflow obstruction?

A

Reversibility testing

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11
Q

What is the differential diagnosis in the event of no airflow obstruction?

A 
Cough syndromes
Hyperventilation
Vocal cord dysfunction
Rhinitis
GORD
Cardiac failure
Pulmonary fibrosis
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12
Q

Which white blood cell is commonly raised in asthma?

A

Eosinophils

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13
Q

Which drugs may stimulate an asthma attack?

A

Beta blockers

Aspirin in 2-3 percent of asthmatics

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14
Q

What is the identifying feature in bronchiectasis?

A

Chronic productive cough

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15
Q

How is bronchiectasis diagnosed?

A

High resolution CT

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16
Q

What is the most common cause of cough with no obvious cough?

A

Acid reflux

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17
Q

What feature of a cough indicates acid reflux?

A

Cough is excessive relative to other asthma symptoms

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18
Q

Is acid reflux cough always with dyspepsia?

A

No

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19
Q

In what percentage of asthmatics is aspirin an irritant?

A

2-3%

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20
Q

What clinical features are associated with aspirin induced asthma?

A

Nasal polyps

Troublesome asthma

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21
Q

What features are commonly seen on the FBC of someone with an exacerbation of asthma?

A

Raised eosinophils and neutrophils

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22
Q

What test may be done to investigate the specific trigger of a patients asthma?

A

Specific IgE finger prick testing

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23
Q

What is the airway responsiveness test?

A

Metacholine challenge

Indirect challenge

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24
Q

What are the methods for primary prevention of asthma?

A

Breastfeeding
Avoid tobacco smoking
?immunotherapy

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25
Q

Is it worth avoiding pathogens for primary asthma prevention?

A

No

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26
Q

What are the risk factors for near fatal asthma?

A

Brittle asthma
Heavy use of beta 2 agonists?
3+ asthma medications

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27
Q

How is acute asthma classified?

A 
Near fatal
Life threatening
Acute severe
Moderate
Brittle
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28
Q

Which patients can be discharged within 1hr?

A

PEF>75% after 1hr unless risk factors or living alone

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29
Q

What are the features of a moderate asthma exacerbation?

A

Increasing symptoms
PEF>50-75% best or predicted
No features of acute severe asthma

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30
Q

What are the features of acute severe asthma?

A

PEF 33-50%
RR greater than or equal to 25/min
HR greater than or equal to 110 bpm
Cannot complete sentences in one breath

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31
Q

What are the features of life threatening asthma?

A

Any one of:

PEF

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32
Q 
What are the clinical features of life threatening asthma?
Normal PCO2
Silent chest
Cyanosis
Feeble respiratory effort
Bradycardi
A 
Normal PCO2
Silent chest
Cyanosis
Feeble respiratory effort
Bradycardia
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33
Q

Describe type 1 brittle asthma?

A

Wide PEF variability (>40% diurnal variation for more than half of the time over 150 days)

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34
Q

Describe type 2 brittle asthma

A

Sudden severe attacks on a background of otherwise well controlled asthma

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35
Q

What is near fatal asthma?

A

Raised PaCO2 and/or requiring mechanical ventilation with raised inflation pressures

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36
Q

What is the principle of near fatal asthma management?

A

Bronchodilators to keep the patient alive/ steroids decrease inflammation

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37
Q

Which bronchodilators should be used in near fatal asthma?

A

Salbutamol or tetrabutaline nebs via spacer
Ipratropium if concerned
iv magnesium

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38
Q

Which bronchodilator should be used if life threatening asthma becomes near fatal?

A

Iv aminophylline

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39
Q

For how longs should steroids be given in acute exacerbations of asthma?

A

5 days

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40
Q

What steroids can be given in severe asthma?

A

Prednisolone 40 or 50 od OR

Hydrocortisone 100 or 200mg qds

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41
Q

How is acute asthma attack managed?

A

ABC
O2 - aim for SaO2 >92%
iv fluids for rehydration and to correct electrolytes

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42
Q

How does FEV1 and FVC change in obstructive disease?

A

FEV1 and FVC reduced so FEV1/FVC reduced

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43
Q

How does FEV1 and FVC change in restrictive disease?

A

Both FEV1 and FVC reduced but FEV1 not reduced as much so FEV1/FVC normal or raised

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44
Q

What is tidal volume?

A

Air expired or inspired in a single breath

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45
Q

What is inspiratory reserve volume?

A

Additional volume of air that can be inspired after tidal volume

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46
Q

What is expiratory reserve volume?

A

Additional volume that can be expired after tidal volume

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47
Q

What is the vital capacity?

A

Maximum volume of air that can be exhaled following max inspiration (IRV+TV+IRV)

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48
Q

How can lung volume be measured?

A

Helium method

Body plethysmography

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49
Q

How is gas transfer measured?

A

CO single breath technique

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50
Q

How does the helium method work?

A

Helium acts as a tracer that mixes with air

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51
Q

What environmental factors are linked to lung cancer?

A 
Pollution
Coal and tar oils
Chromium
Iron oxide
Asbestos
Radiation
Arsenic
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52
Q

Which oncogenes may be present in lung cancer?

A

KRAS, MYC family, EGFR and ALK mutations

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53
Q

Which tumour suppressor genes are relevant to lung cancer?

A

p53

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54
Q

Where can autocrine growth factors be derived from?

A

Nicotine

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55
Q

What percentage of lung cancers are small cell (oat cell) tumours?

A

10%

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56
Q

What types of non small cell lung cancers are there and what is their incidence?

A

Squamous cell carcinoma (20-30%)
Adenocarcinoma (40-50%)
Large cell carcinoma (10-15%)

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57
Q

What are distinctive features of SCLC?

A

May respond to chemo
Endocrine
Often nodal spread
Early aggression - often inoperable

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58
Q

What are features of squamous cell tumours?

A

Typically in smokers
Often cavitates
High serum calcium due to PTH-rp

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59
Q

What are the features of large cell lung cancer?

A

Early metastasis

Undifferentiated

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60
Q

The clinical picture of adenocarcinoma in situ may resemble which other disease?

A

Pneumonia

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61
Q

Which paraneoplastic syndromes are linked to SCLC?

A 
Cushings
Lambert-Eaton syndrome 
Limbic encephalitis
Cerebellar syndrome
Dermatomyositis (more common is SCLC)
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62
Q

Which paraneoplastic syndrome may be present in squamous cell carcinoma?

A

Hypercalcaemia due to PTH-rp

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63
Q

When should an urgent respiratory referral be made?

A

CT/CXR suggests cancer including pleural effusion or slow removal of consolidation
High suspicion with normal CT/CXR
Persistent haemoptysis in smokers/ex-smokers older than 40 years of age OR signs of SVCO obstruction or strider

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64
Q

Why should an MRI be done?

A

To look for pan coast tumours

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65
Q

What is the ideal pathway in the diagnosis of lung cancer?

A 
Patient presents to GP or A&E
CXR abnormal
Refer to respiratory
Respiratory physician requests CT
CT given with report to team
PET scan
Bronchoscopy/ CT biopsy/ EBUS
Histology and PET report
Decide on chemo/ radio/ surgery
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66
Q

What are the symptoms of pleuritic disease?

A 
Asymptomatic
Dry cough
Breathlessness
Pleuritic chest pain
Shoulder pain and heaviness
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67
Q

What is an exudate fluid?

A

More that 30g/l protein in the fluid

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68
Q

What is a transudate fluid?

A

Less that 30g/l protein in the fluid

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69
Q

When should Light’s criteria be used to differentiate between transudate and exudate?

A

If the fluid is between 25g/l and 35g/l

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70
Q

What is Light’s criteria?

A

The fluid is an exudate if:
Pleural fluid/serum protein > 0.5
Pleural fluid LDH/ serum LDH > 0.6
Pleural fluid LDH > 2/3 of upper limit of serum LDH

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71
Q

What can lead to an exudate fluid?

A 
Parapneumonic effusion
Malignancy
PE
Rheumatoid arthritis
Mesothelioma
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72
Q

What conditions can lead to a transudate fluid?

A 
Left ventricular failure
Cirrhotic liver disease
Peritoneal dialysis
Nephrotic syndrome
Constrictive pericarditis
Hypothyroidism
Meig's syndrome
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73
Q

What is a pleural infection?

A

Parapneumonic effusion/empyema

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74
Q

How should pleural effusion be investigated? (After CXR)

A

Diagnostic pleural tap

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75
Q

What other investigations should be done after a pleural tap when investigating pleural effusion?

A

Blood culture
USS
CT chest

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76
Q

What is the most cause of community acquired pleural infection?

A

Streptococcus

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77
Q

What is the second most common cause of community acquired pleural infection?

A

Anaerobes

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78
Q

What is the third most common cause of community acquired pleural infection?

A

Staph aureus

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79
Q

What is the most common cause of hospital acquired pleural infection?

A

Staph - MRSA (25%) and S.aureus (10%)

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80
Q

How should a pleural infection be managed?

A

First line- antibiotics
Seconds line- chest tube drainage
Third line- intrapleural fibrinolytics (not routinely used)
Nutritional support
If still doesn’t resolve refer to surgeons for VATS/thoracotomy and decortication/open thoracic drainage

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81
Q

What is a mesothelioma?

A

Malignant tumour of the serosal surfaces

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82
Q

What is the average latency period of mesothelioma?

A

40 years

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83
Q

What is the prognosis after mesothelioma diagnosis?

A

Poor 9-12 months

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84
Q

What causes a mesothelioma?

A

Asbestos exposure

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85
Q

What signs and symptoms are seen in mesothelioma?

A

Dull ache in chest
Pleural effusion
Weight loss and fatigue
Chest wall invasion

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86
Q

What are the first line investigations in suspected mesothelioma?

A

CXR and CT thorax

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87
Q

What further investigations may be done when investigating mesothelioma?

A

Pleural fluid analysis (cytology and colour)
Biopsy
Histological subtyping

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88
Q

What histological subtypes may be seen in mesothelioma?

A

Epitheloid - 50% - better prognosis
Mixed (biphasic)
Sarcomatoid

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89
Q

Which histological subtype of mesothelioma is the most common and results in the best prognosis?

A

Epithelial

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90
Q

How can pleural effusions be managed?

A

Drainage (pleurodesis if recurrent)

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91
Q

What is the role of radiotherapy in mesothelioma management?

A

Reduce chest wall invasion risk?

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92
Q

Which chemotherapy agents should be used in mesothelioma?

A

Cisplatin + pemetrexed/ gemcitibine

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93
Q

What CXR findings may one see in mesothelioma?

A

Pleural plaques

Basal thickening

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94
Q

What is bronchiectasis?

A

Permanent dilation of the bronchi and bronchioles with necrosis of their walls

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95
Q

What causes bronchiectasis?

A

Obstruction or childhood viral pneumonia

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96
Q

What is a key clinical finding in bronchiectasis?

A

Foul smelling pus

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97
Q

How is bronchiectasis diagnosed?

A

High resolution CT scan

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98
Q

Why does foul smelling pus occur in bronchiectasis?

A

Air ways become sac like and fill with pus

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99
Q

What are the characteristics of the fluid in pulmonary oedema?

A

Pink and granular with haemosiderin-laden macrophages (heart failure cells)

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100
Q

What process occurs in long standing pulmonary oedema?

A

Resolution or ‘brown induration’

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101
Q

What causes ARDS?

A

Diffuse alveolar damage and build up of oedema due to injury to alveolar capillary endothelium

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102
Q

What does histology show in ARDS?

A

Oedema and fluid
Fibrinous membranes lining alveoli
Proceeds to severe scarring

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103
Q

Why is ARDS life threatening?

A

Rapidly developing respiratory insufficiency

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104
Q

Which type of PE is immediately life threatening?

A

Large saddle emboli - lodges are in the bifurcation of the pulmonary trunk

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105
Q

What shape of infarct appears in the lungs in the event of a normal PE?

A

Wedge shaped

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106
Q

Does pulmonary circulation normally have a high or low resistance?

A

Low

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107
Q

What can cause pulmonary hypertension?

A

COPD
Left heart valvular disease
Recurrent thromboemboli

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108
Q

What complication arises from pulmonary hypertension?

A

Right ventricular hypertrophy - chronic cor pulmonale

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109
Q

Which type of lung disease does occupational lung disease normally cause?

A

Restrictive

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110
Q

What are the features of coal workers pneumocosis?

A

Anthracosis
Macules
Progressive massive fibrosis

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111
Q

In what jobs is silicon exposure common?

A

Sandblasting

Foundry work

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112
Q

Which disease are due to silicon?

A

Silicosis

Caplan’s syndrome

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113
Q

Which conditions are linked to asbestos exposure?

A 
Asbestosis
Pleural plaques
Caplan's syndrome
Mesothelioma
Lung, stomach and colon cancer
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114
Q

Which lung disease are due to organic dusts?

A

Farmer’s lung
Baggassosis
Byssinosis
Bird breeder’s lung

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115
Q

Which habit typically causes chronic bronchitis and emphysema?

A

Smoking

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116
Q

What is centriacinar emphysema?

A

Central and proximal parts of the respiratory bronchioles affected and the distal parts are spared
This type is seen in smokers

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117
Q

What is paracinar emphysema?

A

Uniform dilation of acini from respiratory bronchiole to alveoli
Seen in alpha 1 anti trypsin deficiency

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118
Q

Which type of emphysema is seen in alpha 1 anti trypsin deficiency?

A

Paracinar

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119
Q

What is paraseptal emphysema?

A

Peripheral along large margins
Occurs adjacent to scarring/collapse/fibrosis
Predisposition to spontaneous pneumothorax in young adults

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120
Q

Which type of emphysema predisposes young adults to pneumothorax?

A

Paraseptal

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121
Q

What is irregular emphysema?

A

Irregular involvement of acini - linked to scarring

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122
Q

What is the pathogenesis of emphysema?

A

Protease-antiprotease hypothesis

Smoking and congenital alpha 1 anti trypsin deficiency leads to antielastase

Smoking and emphysema leads to elastic damage

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123
Q

Compare chronic bronchitis to emphysema?

A

Chronic bronchitis:
Productive cough for longer than 3m in 2 consecutive years
Mucous gland hypertrophy and hypersecretion +/- infection
Progressive
Hypoxia, hypercapnia and cyanosis prone
Blue bloater

Emphysema:
Permanent dilation of airways distal to terminal bronchiole
Elastic destruction leading to loss of elastic recoil
Centriacinar/paracinar/paraseptal/irregular
Tendency to hyperventilate but ABG normal
Pink puffer

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124
Q

What is the pathogenesis of lung cancer?

A
  1. Normal respiratory epithelium (pseudo stratified columnar, ciliated, mucous secreting)
  2. Turns to stratified squamous
  3. Turns to squamous dysplasia
  4. Becomes carcinoma
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125
Q

What causes hypercapnia?

A

Hypoventilation

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126
Q

What can cause type 1 respiratory failure?

A

Low inspired oxygen
V/Q mismatch - reduced Q e.g PE
Diffusion abnormality e.g pulmonary fibrosis or emphysema in COPD

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127
Q

What can cause type 2 respiratory failure?

A

Thoracic cage problems e.g. obesity, thoracoplasty and kyphoscoliosis
Hyperexpanded lungs e.g. COPD
Obstructive airway disease e.g. COPD or asthma
Weakness of respiratory muscles e.g. MND, DMD

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128
Q

What is CPAP?

A

Continuous positive airway pressure that pushes air into lungs during expiration
It can expand collapsed portions of lung that are underventilated

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129
Q

What improvements are seen with CPAP?

A

Improves V/Q mismatch
Hypoxia
Keeps airway open in sleep apnoea

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130
Q

What is not improved with CPAP?

A

Hypoventilation

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131
Q

Why should too much O2 not be given in type 2 respiratory failure?

A

It will worsen hypoventilation so will worsen hypercapnia

132
Q

How should oxygen be given in type 2 respiratory failure?

A

0.5 to 2.0l via nasal cannula with or 24 to 28% with Venturi mask

133
Q

What is the target saturation in respiratory failure?

A

88 to 92 percent

134
Q

What is non-invasive ventilation?

A

Improves hypoventilation
Delivers high pressure during inspiration to improve ventilation
Improves hypoxia
Reduces hypercapnia
Useful in hypoventilation and type 2 respiratory failure

135
Q

What are the consequences of type 2 respiratory failure?

A 
Poor sleep
Fatigue
Neuro/psychiatric
Secondary polycythaemia leading to stroke
Pulmonary hypertension 
Peripheral oedema
Cor pulmonale
136
Q

What are the complications of chronic hypoxia?

A

Cor pulmonale

Polycythaemia

137
Q

How should acute type 1 respiratory failure be managed?

A

High flow oxygen
60 to 100 percent oxygen via mask
Keep sats above 95 percent
Treat underlying cause

138
Q

When should CPAP be considered in type 1 respiratory failure?

A

Continuing hypoxia

139
Q

How is sleep apnoea diagnosed?

A

Home sleep study

140
Q

What is the definition of obstructive sleep apnoea?

A

Repetitive episodes of partial or complete upper airway obstruction during sleep

141
Q

What is apnoea?

A

Complete stop in airflow for 10s

142
Q

What is hypopnoea?

A

Reduction in airflow by 50 percent or by 30 percent for at least 10s with desaturation of at least 4 percent

143
Q

What is the AHI? (Same as Sleep Disturbance Index)

A

Number of apnoeas or hypopnoeas per hour of the study

144
Q

What are the classifications of the AHI?

A

0 to 5 is normal
5 to 15 is mild
15 to 30 is moderate
30 plus is severe

145
Q

What BMI is linked to OSA?

A

Greater than 30

146
Q

What are the relevant risk factors for OSA?

A 
Obesity - narrows the upper airway
Micrognathia 
Afrocarribean
Neck circumference > 16.5
Tonsillar hypertrophy
Male - longer pharyngeal airway
Acromegaly
Down's syndrome
147
Q

Which system conditions are linked to OSA.

A

Hypothyroid
Cushing’s syndrome
Type 2 DM
Hypertension

148
Q

Which scale is associated with OSA?

A

Epworth sleepiness scale

149
Q

Which features in the history are suggestive of OSA?

A 
Snoring
Arousals
Waking unrefreshed
Daytime tiredness
Planned or unplanned naps
Witnessed by partner
150
Q

When should CPAP be used?

A

Moderate or severe OSA

151
Q

When should mandibular splints be advised?

A

Mile to moderate sleep apnoea
Simple snorers
Intolerance to CPAP

152
Q

What is the aetiology of sarcoidosis?

A

Exaggerated immune response

Kveim antigen - mycobacterial catalase peroxidase (Kat G)

153
Q

Which gene is linked to acute sarcoidosis lasting less than 2 years with a better prognosis?

A

DR3

154
Q

Which genes are linked to chronic sarcoidosis?

A

DR14

DR15

155
Q

Which gene is associated with a better response to anti TNF in sarcoidosis?

A

TNF variant

156
Q

Which IL variants may occur in sarcoidosis?

A

IL 12 and IL 23

157
Q

Which other genes are linked to sarcoidosis?

A

ATNXA11 and XAF1

158
Q

What is the main age range for sarcoidosis?

A

25 to 45 years

159
Q

Is SACE raised in sarcoidosis?

A

Yes

160
Q

Is tuberculin raised in sarcoidosis?

A

No

161
Q

Which CXR features are typically seen in sarcoidosis?

A

Bilateral hilar lymphadenopathy

Apical involvement

162
Q

What are the clinical features of sarcoidosis?

A 
80 percent of cases are asymptomatic
Dry cough
Breathlessness
Red eyes
Skin lesions
Thirst and polyuria (due to high calcium)
Arthritis
Neurological
163
Q

How should asymptomatic sarcoidosis be monitored?

A

Monitor lung function and SACE

164
Q

How should symptomatic sarcoidosis be managed?

A

Steroids

165
Q

How is TB diagnosed?

A

Sputum smear

166
Q

What antibiotics are given in TB?

A

Rifampicin

Isoniazid

167
Q

Why does pyrazinamide need to be given with isoniazid?

A

To prevent antibiotic induced peripheral neuropathy

168
Q

What percentage of TB strains are resistant to isoniazid and rifampicin?

A

3.5 percent

169
Q

Which immune cells are linked to post-primary TB?

A

CD4 and CD8

170
Q

What is the mechanism of isoniazid?

A

Bacteriacidal acting on the cell wall

171
Q

How does rifampicin work?

A

Bacteriostatic on cell wall

172
Q

How does pyrazinamide work?

A

Bacteriostatic of FAS11

173
Q

How does ethambutol work?

A

Bacteriostatic on cell wall

174
Q

What is the second line investigation in someone presenting with TB symptoms?

A

Mantoux test if under 35

CXR if over 35

175
Q

What type of granuloma is seen in TB?

A

Caseating granuloma

176
Q

What type of granuloma is present in sarcoidosis?

A

Non caseating granuloma

177
Q

What is the pathophysiology of primary pneumothorax?

A

Air leaks from subpleural blebs and Bullard

178
Q

Which are bullae?

A

Air filled blisters in the visceral pleura

179
Q

What conditions can lead to secondary pneumothorax?

A 
COPD- 60 percent
Asthma
Connective tissue disease e.g. Marfans
Lung fibrosis
TB
CF
180
Q

What are the clinical features of pneumothorax?

A

Acute pleuritic chest pain +- shortness of breath
Reduced chest expansion
Hyperresonance
Subcutaneous emphysema - bubble and crack
Quiet breath sounds
Tachycardia

181
Q

How is a small pneumothorax defined?

A

Less than 2cm on CXR

182
Q

How is large pneumothorax defined?

A

More than or equal to 2cm on CXR

183
Q

How should a small pneumothorax be managed?

A

Conservatively with high flow oxygen and let it reabsorb (happens at a rate of 1.25%)

184
Q

When should a pneumothorax be medically managed?

A

If the rim is greater than 2cm with or without breathlessness

185
Q

How should a large pneumothorax be medically managed?

A

Aspirated with 16-18G cannula up to 2.5l of air this is considered successful if the rim is now less than 2cm and breathing has improved. If the aspiration is not successful a chest drain can be done (the patient should be admitted).

186
Q

How should a chest drain be managed?

A

Underwater seal and drainage
Do not lift above waist to prevent retrograde flow of fluid or air
Do not clamp if bubbling or a tension pneumothorax will develop

187
Q

What are the clinical signs of a tension pneumothorax?

A

Trachea and mediastinum deviate away
Raised JVP
Hypotension
Very breathless

188
Q

How should a tension pneumothorax be managed?

A

Needle decompression with a large bore (14G) needle in the mid clavicular line 2nd intercostal space

189
Q

What is a PE?

A

Thrombi from a distant site

190
Q

What percentage of post operative deaths are due to PE?

A

15%

191
Q

What is the most common cause of maternal death?

A

PE

192
Q

What percentage of thrombi are formed in the deep veins of the lower limb and pelvis?

A

75 percent

193
Q

In which veins do thrombi develop?

A

Deep veins of the lower limb and pelvis

194
Q

What is the pathophysiology of PE?

A

Thrombi formed in the deep veins of the pelvis and lower limb
Platelet aggregation around venous valve sinuses
Clotting cascade activated

195
Q

What is Virchow’s triad?

A

Injury to vessel wall
Venous stasis
Increased coagulability

196
Q

What can cause PE?

A 
Acute illness
Immobility
Air travel
Trauma
Pregnancy 
Oestrogen
Malignancy
Hereditary/acquired thrombophilia
197
Q

How is a PE diagnosed?

A

CTPA

198
Q

What test should be done in the event of a chronic PE?

A

V/Q scan (lower radiation)

199
Q

What should be done prior to PE management?

A

Wells Score

200
Q

What are the components to the Wells score?

A 
Clinical DVT (3 points)
PE most likely diagnosis (3 points)
HR over 100 (1.5 points)
Immobilisation for 3 days or surgery in the last 4 weeks (1.5 points)
Previous DVT/PE (1.5 points)
Haemoptysis (1 point)
Malignancy with treatment in the last 6m (1 point)
201
Q

How should a wells score be graded?

A

Score over 4 - consider imaging

Score under 4 - rule out PE with a normal D-dimer

202
Q

What findings may show on an ECG with PE?

A

Sinus tachycardia
RBBB
RV strain (anterior T wave inversion)
S1 Q3 T3

203
Q

What is the medical management of PE?

A

Anticoagulation with LMWH or warfarin

Thrombolysis

204
Q

What is the interventional radiology management for PE?

A

Inferior vena cava filter

205
Q

What is the surgical management if PE?

A 
Embolectomy (if life threatening)
Pulmonary thromboendarterectomy (chronic PE)
206
Q

What are the presenting features of a large PE?

A

Hypotension, collapse and cardiac arrest
Acute right heart strain
Right heart failure

207
Q

What are the features of acute right heart strain?

A

Loud P2
Splitting of 2nd heart sounds
Gallop rhythm

208
Q

What are the features of right heart failure?

A

Raised JVP
Low BP
Low cardiac output

209
Q

What are the presenting signs of a PE?

A 
Normal
Sinus tachycardia
New onset AF
Reduced chest movement due to pain
Pleural rub
Pleural effusion
DVT
SOB
Low grade fever
Collapse
210
Q

What are the presenting symptoms of COPD?

A 
Exertional  breathlessness
Chronic cough
Regular sputum production and frequent chest infections
Frequent winter bronchitis
Wheeze
211
Q

How is COPD diagnosed?

A

Post bronchodilator spirometry- not much change in FEV1

212
Q

What are the stages of COPD?

A

Stage 1 - mild - 80 percent with symptoms
Stage 2 - moderate - 50-79 percent
Stage 3 - severe - 30-49 percent
Stage 4 - very severe - below 30 percent ( or less than 50 percent with respiratory failure)

213
Q

Why is it necessary to do a CXR when diagnosing COPD?

A

To rule out other causes

214
Q

What further investigations should be done in COPD? After CXR

A

ABG for respiratory failure and acidosis
FBC to look for anaemia or polycythaemia
BMI calculation

215
Q

Which genetic factor may cause COPD or emphysema in younger patients?

A

Alpha 1 anti trypsin deficiency

216
Q

What is the first line management in COPD?

A

Lifestyle changes
Reduction in risk factors such as the pneumococcal and influenza vaccine
Chest physiotherapy if needed
Short acting antimuscarinic (Ipratropium) or beta 2 agonist (salbutamol) PRN

217
Q

Which bacteria is most likely to cause an acute exacerbation of COPD?

A

H. Influenzae

218
Q

How should mild to moderate COPD be managed?

A

Inhaled long acting muscarinic (tiotropium) or beta 2 agonist

219
Q

How should severe COPD be managed?

A

Combination long acting beta 2 agonist and corticosteroids (budesonide + formoterol) or tiotropium

220
Q

If severe COPD remains symptomatic, what is the second line treatment?

A

Tiotropium + inhaled steroid + long acting beta 2 agonist

Consider steroid trial, home nebs and theophylline

221
Q

How can pulmonary hypertension in COPD be managed?

A

Assess the need for long term oxygen therapy

Treat oedema with diuretics

222
Q

What theoretically can cause asthma?

A 
Air pollution
Allergen exposure
Maternal smoking
Dietary changes
Hygiene hypothesis
Genetics - there is an inheritable component
223
Q

Which non-pharmacological treatments have been proven effective in asthma?

A

Weight control
Avoid smoking
Buteyko

224
Q

What is the first step in asthma treatment (mild intermittent asthma)?

A

Short acting beta agonist PRN e.g. salbutamol, terbutaline

225
Q

What is the second step in asthma management (regular preventer therapy)?

A

Inhaled steroid 200-800 mcg but 400mcg is a good starting dose e.g. beclamethasone, budenoside, fluticasone

226
Q

What is the third step in asthma management? (Initial add on therapy)

A

Add LABA e.g. Salmeterol or formoterol
if there is not a full benefit from LABA increase inhaled steroid dose to 800mcg
If no response to LABA increase inhaled steroids to 800mcg and try leukotriene antagonist or SR theophylline

227
Q

What is the fourth step in asthma management? (Persistent poor control)

A

Consider trials of increasing inhaled steroids to 2000mcg

Add fourth drug e.g. Leukotriene receptor agonist, SR theophylline, beta 2 agonist tablets

228
Q

What is step 5 in the management of asthma?

A

Daily steroid tablets
Consider ways to minimise steroid use
Refer to respiratory

229
Q

What has shown to decrease asthma mortality?

A

Increased corticosteroid use

230
Q

Give an example of a leukotriene receptor antagonist

A

Monteleukast

231
Q

What is the mechanism of action of theophylline?

A

Phosphodiesterase inhibitor

232
Q

What are the indications for anti-IgE therapy?

A 
On maximum inhaled therapy
Impaired lung function
Symptomatic
Frequent exacerbations especially due to allergy
Raise IgE but less than 700iu/litre
233
Q

How does Anti IgE therapy work?

A

Monoclonal antibody that decreases free IgE

234
Q

Give an example of anti IgE therapy

A

Omalizumab

235
Q

How is anti IgE therapy given?

A

2-4 weekly subcutaneous injections

236
Q

What is upper airways disease?

A

Asthma +- sinusitis or rhinitis (often coexist)

237
Q

What factors can precipitate asthma?

A 
Viral infection
Dust/ house mites
Animal dander
Pollen
Smoke/ pollution
Exercise
Atmospheric conditions
238
Q

Which lung diseases show a restrictive pattern?

A 
Pleural
Alveolar
Interstitial
Neuromuscular
Thoracic cage
239
Q

What is the vital capacity?

A

Maximum volume of air that can be exhaled following a maximal inspiration (VC = IRV + TV + ERV)

240
Q

What is the inspiratory capacity?

A

Volume of air that it is possible to inspire at the end of a normal quiet expiration? (IC = TV + IRV)

241
Q

What is the residual volume?

A

Volume of air remaining in the lungs and airways at the end of a maximal expiration?

242
Q

What is the functional residual capacity?

A

Volume of air contained in the lungs at the end of a quiet tidal volume expiration (FRC = RV + ERV)

243
Q

What is the total lung capacity?

A

The volume of air contained in the lungs at the end of a maximal inspiration (TLC = RV+ERV+TV+IRV)

244
Q

What is Lambert Eaton syndrome? (Can be paraneoplastic in SCLC)

A

Myaesthenic autoimmune disease where the immune system attacks the neuromuscular junction

245
Q

In TNM staging what is a T1a tumour?

A

Small peripheral tumour which can be removed surgically

246
Q

What grade is given to a large invading tumour?

A

T4

247
Q

What is an N1 tumour?

A

Hilar lymph node involvement

248
Q

What is an N2 tumour?

A

Mediastinal lymph node involvement

249
Q

What is an N3 grade cancer?

A

Contractural lymph node involvement

250
Q

What is a grade M1a lung cancer?

A

Metastatic pleural effusion

251
Q

What is a grade m1b tumour?

A

Mets at common sides such as liver, lungs, adrenals, brain, bones

252
Q

What are the complications of radiotherapy?

A

Early-radiation pneumonitis

Late-fibrosis

253
Q

Why may palliative radiotherapy given in lung cancer?

A

To relieve pain and to stop haemoptysis and neurological problems through brain and spinal mets

254
Q

What is the survival advantage when giving chemo in lung cancer?

A

Small

255
Q

Which chemotherapy agents are given in small cell lung cancer?

A

Pemetrexed and cisplatin

256
Q

What other agents may be combined with chemo in lung cancer?

A

EGFR antagonists such as endotinib

257
Q

What palliative treatments can be given in lung cancer?

A 
Endobronchial laser to relieve obstruction, breathlessness and haemoptysis
Stenting to relieve breathlessness
Endobronchial radiotherapy (brachytherapy)
258
Q

Why type of fluid do disease affecting local factors in the lung produce?

A

Exudate

259
Q

What type of fluid do diseases affecting systemic factors produce?

A

Transudate

260
Q

Which diseases affect local factors in the lung and what conditions do they produce?

A

Increased capillary permeability - trauma, malignancy, inflammation, infection, pancreatitis
Increased pleural permeability - inflammation, malignancy and PE
Decreased lymphatic drainage - malignancy and trauma
Increased negative pleural pressure - atelectasis, mesothelioma

261
Q

Which systemic factors affecting the lung are affected by which disease?

A

Increased capillary hydrostatic pressure - heart failure
Increased pulmonary interstitial fluid - heart failure
Decreased intravascular oncotic pressure - hypoalbuminaemia, cirrhosis
Increased flow from other cavities - peritoneal dialysis, liver cirrhosis

262
Q

What is the progression of a pleural infection?

A

Simple parapneumonic effusion to complicated parapneumonic effusion to empyema

263
Q

What are the characteristics of the fluid produced in simple parapneumonic effusion?

A

Clear, sterile fluid with normal pH, glucose and LDH that resolves with LDH
Chest drain not usually required

264
Q

What are the characteristics of the fluid produced in a complicated parapneumonic effusion?

A

Fibrinopurulent stage, fluid infected but not purulent. pH 1000iu/l, gram stain may be positive
Chest drain needed

265
Q

What is the characteristic of the fluid in empyema?

A

Pus in the pleural space, free flowing or multiloculated, fluid gram stain may be positive. Fibroblasts may have cause a thickened pleura.
Drainage required

266
Q

What is the incidence of pneumonia?

A

5 - 11 cases per 1000 adults

267
Q

What is the 30 day mortality of pneumonia?

A

18.3 percent

268
Q

What are symptoms of pneumonia?

A 
Cough
Pleural pain
Dyspneoea
Tachypnoea
Sweating, fevers, shivers, aches, pain, fevers
269
Q

What are the signs of pneumonia?

A

New and focal chest signs

Radio graphic changes - new radio graphic shadowing with no other explanation

270
Q

Do most cases of pneumonia have an unidentified pathogen?

A

Yes

271
Q

What is the most common pathogen in pneumonia?

A

Strep pneumoniae

272
Q

When should healthcare associated pneumonia be considered?

A

Inpatient longer than 48hrs or 10 days post discharge or living in nursing home

273
Q

Which pathogens are common in HAP?

A

H. Influenza, Gram negative bacilli, S.aureus all increased due to aspiration

274
Q

Which pathogens are less likely in HAP?

A

Legionella and unknown pathogens

275
Q

Which pathogens are more common in the elderly?

A

M. pneumonia and legionella

276
Q

How does alcohol influence pneumonia?

A

Increased risk of most pathogens

Aspiration most likely

277
Q

How does diabetes influence pneumonia?

A

Increased risk of bacteraemic pneumococcal pneumonia

278
Q

What impact does COPD have on pneumonia?

A

H.influenza and M.catarrhalis more likely

Increased symptoms but same mortality

279
Q

Which bacteria is almost unseen in HAP?

A

Legionella

280
Q

Which can disrupt filtration and increase deposition in the upper airways?

A

Anatomical abnormalities

281
Q

What can affect the cough reflex leading to increased chance of aspiration?

A

Neurological conditions e.g. stroke

282
Q

What can reduce mucocilliary clearance?

A

Cystic fibrosis

Bronchiectasis

283
Q

What can damage and reduce alveolar macrophages?

A

Alcoholism

284
Q

What reduces humoral and cellular immunity?

A

HIV

285
Q

What can negatively affect the oxidative metabolism of neutrophils?

A

Chemotherapy

286
Q

What are the components of the CURB65 score?

A 
Confusion AMTS less than 8
Urea equal to or greater than 7mmol/l
Respiratory rate greater than 30
BP systolic less than 90/ diastolic less than or equal to 60
65 - age 65 plus
287
Q

How does the CURB65 score influence pneumonia treatment?

A

0-1 treat at home - amoxicillin 500mg tds oral
2 short admission - amoxicillin 500mg tds oral
3 plus admit - urgent senior review amoxicillin 500mg tds oral + clarithromycin 500mg bd oral
4-5 admit into ITU/HDU - coamoxiclav 1.2g tds IV and clarithromycin 500mg bds IV
If legionella expected give levofloxacin

288
Q

What does the trachea consist of?

A

C shaped cartilage

Mucinous glands

289
Q

What do the bronchi consist of?

A

Discontinuous cartilage plates and mutinous glands

290
Q

What do the bronchioles consist of?

A

No cartilage or mucous glands
Terminal bronchioles are less than 2mm in diameter
Gas exchange occurs in the terminal bronchioles

291
Q

What do the alveolar ducts consist of?

A

Flat epithelium, no glands or cilia

292
Q

What do the alveolar sacs consist of?

A

No glands or cilia

293
Q

What does Eisenmeger syndrome consist of?

A

Right to left shunt via VSD
Hypertrophic right ventricle
Patent ductus arteriosus

294
Q

What are the defence mechanisms of the lung?

A

Particles bigger than 10 microns held in the upper airway

3-10 microns held in tracheobronchial mucus (mucocilliary action)

295
Q

Which age group does lobar pneumonia typically affect?

A

Previously healthy males aged 20-50

296
Q

What is the pathophysiology of lobar pneumonia?

A 
Congestion (24hrs) - vessels engorged, oedema in alveoli, heavy red lung
Red hepatisation (2-4d) - outpouring of neutrophils and RBCs into alveoli, red, solid, airless liver like lung
Grey hepatisation (4-8d) - fibrin and macrophages replace neutrophils and RBCs. Grey, solid and airless lung.
Resolution (8-10d) - gradual return to normal
297
Q

What is a serious complication of lobar pneumonia?

A

Lung abscess or empyema especially with Klebsiella or Staph aureus

298
Q

What is the most common type of pneumonia?

A

bronchopneumonia

299
Q

What are the 4 typical clinical settings where bronchopneumonia occurs?

A

Chronic debilitating illness
Old age
Infancy
Secondary to viral infection

300
Q

What is the pathophysiology of bronchopneumonia?

A

Bilateral, basal and patchy progressing to grey/red spots of consolidation and microscopically acute inflammatory infiltrate in bronchioles and alveoli

301
Q

What CXR findings are present in bronchopneumonia?

A

Focal opacities, clinical signs are less pronounced, usually patchy bilateral basal distribution.

302
Q

Which pathogens are typically responsible in bronchopneumonia?

A

Staph, strep viridians, pneumococcus, haemophilia, pseudomonas, coliforms

303
Q

What is atypical pneumonia?

A

Interstitial pneumonia

304
Q

What are the clinical signs of interstitial pneumonia?

A 
Patchy or extensive
Congested and subcrepitant lungs
Secondary bacterial infection
More generalised symptoms rather than local
Usually sporadic
Usually mild and self limiting
Possible DAD (diffuse alveolar damage)
305
Q

What are predisposing conditions to interstitial pneumonia?

A

Malnutrition, alcoholism, debilitating illness

306
Q

What is the pathogenesis of interstitial pneumonia?

A

Intra alveolar proteinaceous material forming hyaline membranes in the case of DAD

307
Q

What is found on histology with interstitial pneumonia?

A

Inflammation restricted to alveolar septa and interstitial pneumonia
No/minimal alveolar exudate

308
Q

What pathogens may be present in interstitial pneumonia?

A 
Mycoplasma pneumoniae
Viruses: influenza A and B, RSV, adenovirus, rhinovirus, rubeola, varicella
Chlamidya 
Coxiella
Often undetermined
309
Q

Which pathogens cause TB?

A

M.tuberculosis

M.bovis

310
Q

What is the pathogenesis of TB?

A

Cell mediated hypersensitivity central to development of characteristic destruction through caseating necrosis and cavitation
Macrophages phagocytose but cannot kill bacteria so they multiply, lyse and infect other cells
T cell mediated immunity 2-3 weeks post infection:
CD4 mediated IFN gamma secretion intracellular killing and granuloma formation
CD8 mediated lysis of macrophages and killing
CD4-/CD8- mediated lysis of macrophages and caseation and necrosis; bacilli killed in an anoxic, acidic environment

311
Q

What is primary TB?

A

Represents first reponse to tubercle bacili

Usually asymptomatic

312
Q

What is the pathophysiology of primary TB?

A

Ghon complex (typically 1cm focus in midzone with draining lymph node) that leads to fibrosis and calcification

313
Q

What is the pathophysiology of secondary TB?

A

Reinfection or reactivation, sometimes progressive primary TB
Bacteria relocate to high oxygen areas of the lung
Usually apical granuloma 3cm at presentation

314
Q

Which type of hypersensitivity is relevant to primary TB?

A

Type IV (delayed type)

315
Q

What can be seen on histology with TB?

A

Granulomas with caseous necrosis
Langhans giant cells
Epitheloid macrophages

316
Q

What does a Ziehl-Neelsen stain reveal with TB?

A

Characteristic acid-fast bacilli

317
Q

What are the complications of pulmonary TB?

A

Progressive fibrocavitary TB - gradually destroys lung through necrosis, cavitation and fibrosis
Miliary TB - blood bourne dissemination within lung or throughout the body, seed like foci consisting of granulomas in meninges, bone marrow, liver or any other organ

318
Q

Which patients get fungal pneumonia?

A

Immunocompromised

319
Q

Which fungi is responsible for fungal pneumonia in HIV patients?

A

Pneumocystis carinii (PCP)

320
Q

What is the human response to primary TB?

A 
No pre existing immunity
Non infectious
High mortality 
Often outside lung
Children and elderly
HIV co infection
321
Q

What is the human response to post primary TB?

A 
Pre existing immunity
Infectious
Cavities with TB biofilm
Surprisingly well tolerated
Young adults effected
Immunocompetent with CD4 and CD8 involvement
322
Q

What are the side effects if isoniazid?

A

Liver damage - raised ALT
Peripheral neuropathy
Nausea
Tiredness

323
Q

What are the side effects of rifampicin?

A

Liver damage - raised bilirubin
Flu like syndrome
Low platelets

324
Q

What are side effects of pyrazinamide?

A

Flushing
Arthritis
Liver damage

325
Q

What are the side effects of ethambutol?

A

Optic neuritis

Cardiorespiratory (3 decks)

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