Respiratory Flashcards

1
Q

What is a common organism which causes pneumonia in bird owners?

A

chlamydia psittaci

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2
Q

cavitating pneumonia in the upper lobes, mainly in diabetics and alcoholics suggest what?

A

Klebsiella pneumoniae

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3
Q

Long term use of what can precipitate restrictive lung disease?

A

Nitrofurantoin

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4
Q

Which condition is immune deficiencies such as hypogammaglobulinemia associated with?

A

Bronchiectasis

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5
Q

What type of picture do you get on pulmonary function testing in asbestosis?

A

Restrictive - FEV1 goes down, FVC goes down A LOT therefore overall FEV1/FVC increases

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6
Q

What is the investigation of choice for occupational asthma?

A

Peak flows at work and home

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7
Q

What is the pathogen involved in Farmer’s lung?

A

Saccharopolyspora rectivirgula

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8
Q

Chlamydophila psittaci is associated with what?

A

Contact with birds

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9
Q

How should any critically ill patient be managed with oxygen?

A

15L high flow oxygen via non-rebreather as hypoxia kills before hypercapnia

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10
Q

What should you aim for in step down treatment of asthma?

A

reduction of 25-50% in the dose of inhaled corticosteroids

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11
Q

pulmonary fibrosis predominantly affecting the lower zones

A

Asbestosis

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12
Q

How would opiate overdose present on blood gas?

A

Respiratory acidosis

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13
Q

Redcurrant jelly sputum is found in what?

A

Klebsiella pneumonia

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14
Q

What is the COPD exacerbation treatment?

A
  1. Give O2 if <90%; Venturi 24% mask at 2-3l or nasal cannula flow rate 1-2l/min; Target oxygen sats 88-92%
  2. Nebulised bronochodilators: salbutamol (beta adrenergic agonist) or ipratropium (muscarinic antagonis)
  3. Steroid therapy: 30mg oral pred od for 5d or IV hydrocortisone
  4. Consider need for Abx: amoxicillin 500mg 3x d for 5d (or clarithromycin or doxy) or if at high risk of treatment failure then co-amoxiclav 500/125mg 3xd for 5d
  5. IV Theophylline if not responding to bronchodilators
  6. Non invasive ventilation e.g. BIPAP (if develop T2resp failure)
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15
Q

Why does hypotension occur in tension pneumothorax?

A

Cardiac outflow obstruction

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16
Q

Most common organism causing infective exacerbation of COPD?

A

H influenzae

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17
Q

30-40 year old with basal emphysema and abnormal LFTs

A

Alpha-1-antitrypsin deficiency

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18
Q

Fine end-inspiratory crepitations

A

pulmonary fibrosis

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19
Q

Investigation of choice for sleep apnoea?

A

Polysomnography

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20
Q

Coal workers’ pneumoconiosis causes what?

A

Upper zone fibrosis

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21
Q

What should be sent with diagnostic pleural taps?

A
  • Biochemistry to determine protein
  • Cytology
  • Microbiology for gram staining and culture
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22
Q

What is important to remember about lung cancers?

A

Lesion can sometimes be too small to see on CXR

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23
Q

Paratracheal lymph nodes should raise alarm bells for?

A

Lung cancer

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24
Q

Sarcoidosis can cause what?

A

Hypercalcaemia

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25
Q

What is atelectasis?

A

A post op complication when the airways become blocked by bronchial secretions leading to respiratory collapse
- Managed with chest physio and positioning the patient upright

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26
Q

Normal/raised total gas transfer with raised transfer coefficient

A

Asthma

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27
Q

Lung collapse vs pleural effusion on CXR?

A

Lung collapse - trachea pulled towards the side of the white out
Pleural effusion - trachea pulled away from the side of the white out

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28
Q

Management of bronchiectasis?

A

Muscle training + postural drainage techniques

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29
Q

Patients who have frequent COPD exacerbations should have home supply of what?

A

Abx plus prednisolone

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30
Q

Investigation of choice for pulmonary fibrosis?

A

High res CT

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31
Q

Pack years formula

A

No of packs per day (1 pack is 20) x no of years smoking

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32
Q

Everyone over the age of 5 should have what to diagnose asthma?

A

Spirometry with bronchodilator reversibility testing

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33
Q

ENT, respiratory and kidney involvement

A

Think of Granulomatosis with polyangiitis

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34
Q

A negative result on spirometry does not what?

A

Exclude asthma -> FeNO testing needed

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35
Q

What pattern on lung function does bronchiectasis have?

A

Obstructive

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36
Q

When should Abx be given for COPD exacerbation?

A
  • If purulent sputum or signs of pneumonia
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37
Q

Facial rash plus lymphadenopathy

A

Sarcoidosis

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38
Q

Cavitating lesions are associated with what?

A

Squamous cell carcinoma

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39
Q

increased FEV1/FVC ratio and reduced transfer factor

A

Pulmonary fibrosis

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40
Q

Which paraneoplastic syndrome is associated with squamous cell carcinoma?

A

Parathyroid hormone related protein secretion

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41
Q

Decrease in pO2/FiO2 in poorly patient with non-cardiorespiratory presentation

A

ARDS

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42
Q

Neuromuscular disorders present how on pulmonary function tests?

A

Restrictive pattern

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43
Q

How is asthma diagnosed on spirometry?

A

Improvement in FEV1 by > 15% following administration of bronchodilator

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44
Q

How does salbutamol work?

A

Stimulates ß2 receptors of respiratory tract, which increases sympathetic activity and relaxes bronchial smooth muscle.

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45
Q

What physiological measurement is used to determine the severity
of COPD?

A

FEV1

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46
Q

What must patients do to qualify for long term oxygen therapy?

A

Stop smoking

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47
Q

What are some examination signs of consolidation?

A

Reduced chest expansion, dull percussion note, increased tactile
vocal fremitus, increased vocal resonance, bronchial breathing.

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48
Q

Why should statins and macrolides not be given together?

A

Increased risk of myositis

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49
Q

What are some complications of pneumonia?

A
  • Resp failure
  • Sepsis
  • Empyema
  • Lung abscess
  • Shock
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50
Q

How would pleural effusion present on examination?

A
  • Reduced chest expansion
  • Stony dull to percuss
  • Reduced breath sounds
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51
Q

How would pneumothorax present on examination?

A
  • Reduced chest expansion
  • Hyper resonant on percussion
  • Reduced breath sounds
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52
Q

What is an indication for surgery in bronchiectasis?

A

If the disease is localised to one lobe

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53
Q

Massive PE + hypotension

A

Thrombolysis

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54
Q

What is used to guide if patients need Abx with acute bronchitis?

A

CRP levels - if >100 -> offer Abx

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55
Q

multiple lip telangiectases

A

Think hereditary haemorrhagic telangiectasia -> strong association with epistaxis

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56
Q

Investigation of choice for suspected PE in someone with renal impairment?

A

V/Q scan

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57
Q

When should LTOT be started for COPD patients?

A

When 2 measurements of pO2 are < 7.3
pO2 of 7.3 - 8 AND polycythaemia/peripheral oedema/pulmonary HTN

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58
Q

Causes of upper zone fibrosis

A

C - coal workers pneumoconiosis
H - histiocytosis
A - ankylosing spondylitis
R - radiation
T - TB
S - Silicosis/Sarcoidosis

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59
Q

Causes of lower zone fibrosis

A

D - drugs
A - asbestosis
I - idiopathic
M - Most connective tissue disorders except AS

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60
Q

Non-obs based admission criteria for asthma?

A
  • Previous near fatal attack
  • Pregnancy
  • Oral steroids not helping with symptoms
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61
Q

Bilateral parotid gland swelling can be indicative of what?

A

Sarcoidosis

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62
Q

What are some complications of bronchiectasis?

A

Pneumonia, sepsis, recurrent infections, resp failure

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63
Q

What is the mechanism of PE?

A

T1 Resp failure due to V/Q mismatch

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64
Q

Pemberton’s test

A

Test for SVC obstruction - raise arms above head and they go cyanosed

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65
Q

Non respiratory causes of pulmonary fibrosis

A
  • Amiodarone, methotrexate
  • RA
  • SLE
  • Sjogrens
  • UC
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66
Q

ECG signs of cor pulmonale

A
  • right axis deviation
  • P pulmonale
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67
Q

Causes of bilateral hilar lymphadenopathy

A

Lymphoma, TB, Sarcoidosis, bronchial carcinoma

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68
Q

What are extra-pulmonary manifestations of sarcoidosis?

A
  • Erythema nodosum
  • Anterior uveitis
  • Neuropathy
  • Cardiomyopathy
  • CN palsies
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69
Q

Where should pleural tap needle be inserted?

A

Above rib to avoid neurovascular bundle

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70
Q

What could an area of dull to percuss in someone with a pneumothorax suggest?

A

Haemothorax -> needs chest drain

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71
Q

Lung cancer can present as what?

A

SVC obstruction

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72
Q

What helps to reduce mortality in someone with ARDS?

A

Low tidal volume mechanical ventilation

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73
Q

Uncompensated type 2 resp failure with pH <7.35

A

Think about non invasive ventilation

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74
Q

Radiation exposure can cause what?

A

Lung cancer

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75
Q

What is the pathophysiology of ARDS?

A

Diffuse bilateral alveolar injury due to inflammation

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76
Q

Previous history of haemorrhagic stroke at any time is a C/I to what?

A

Thrombolysis

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77
Q

Excessive daytime sleepiness with visual hallucinations

A

Narcolepsy -> multiple sleep latency test needed

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78
Q

What is PERC criteria used for?

A

To rule out PE

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79
Q

What are indications for steroids in sarcoidosis?

A

PUNCH
Parencymal lung disease
Uveitis
Neuro involvement
Cardio involvement
Hypercalcaemia

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80
Q

Large round well circumscribed masses in the lungs?

A

Cannonball metastases -> renal cell carcinoma

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81
Q

Investigations for lung cancer?

A
  1. CXR
  2. CT with contrast
  3. Bronchoscopy
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82
Q

Raised platelets can be a sign of what?

A

Lung cancer

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83
Q

When are Abx used in acute bronchitis?

A

If there are existing co-morbidities

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84
Q

Preceding influenza predisposes you to what?

A

Staph aureus pneumonia

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85
Q

What is the treatment for latent TB?

A

3 months of isoniazid and rifampicin or 6 months of isoniazid

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86
Q

How should patients with acute asthma who do not respond to medical treatment and become acidotic be managed?

A

Intubation and Ventilation

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87
Q

Where should needle thoracostomy be placed?

A

cannula into the second intercostal space in the midclavicular line on the affected side

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88
Q

egg shell calcification of lymph nodes?

A

Silicosis

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89
Q

What are causes of resp alkalosis?

A
  • Anxiety
  • PE
  • Stroke, sub arachnoid
  • Altitude
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90
Q

What are causes of resp acidosis?

A
  • COPD
  • Neuromuscular disease
  • Sedating drugs like benzos/opiates
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91
Q

Pneumothorax management

A
  1. Asymptomatic -> conservative care
  2. If symptoms and high risk -> chest drain
  3. If symptoms and not high risk -> can manage conservatively/needle aspiration
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92
Q

How should pneumothorax be followed up when managed conservatively?

A
  1. If primary -> review every 2-4 days as outpatient
  2. If secondary -> monitor as inpatient
  3. Everyone should be reviewed in outpatients in 2-4 weeks
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93
Q

CURB65 criteria

A

Confusion
Urea > 7
RR > 30
BP <90 systolic or <60 diastolic
Aged > 65

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94
Q

Community acquired pneumonia treatment

A

0 - treat at home - Amoxicillin/Clarithromycin
1-2 - consider hospital - Amoxicillin + Clarithromycin
3-4 - urgent hospital - Co-amoxiclav or
+ Clarithromycin

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95
Q

Hospital acquired pneumonia treatment

A

No severe signs: Co-amoxiclav
Sever signs: Piperacillin with Tazobactam

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96
Q

Exudate vs Transudate pleural effusion

A

Exudate - >30
Transudate - <30

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97
Q

What are exudative causes of pleural effusion?

A
  • Pneumonia
  • RA/SLE
  • Neoplasia
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98
Q

What are transudative causes of pleural effusion?

A
  • HF
  • Liver disease
  • Hypothyroidism
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99
Q

How to diagnose mesothelioma?

A
  • CXR
  • Pleural CT with biopsy
  • Thoracoscopy can be used
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100
Q

Types of non small cell lung cancer?

A
  • Large cell
  • Squamous cell
  • Adenocarcinoma
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101
Q

What paraneoplastic features do lung cancers have?

A

Small cell
- SIADH
- Cushings
- Lambert-Eaton

Squamous
- PTHrP
- Hypercalcaemia
- Hypertrophic pulmonary osteoarthropathy

Adenocarcinoma
- Gynaecomastia

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102
Q

How long should patients hold breath when taking inhaler?

A

10 seconds after pressing down on cannister
Wait 30 seconds before repeating next dose

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103
Q

What is Churg Strauss syndrome?

A

Eosinophilic granulomatosis with polyangiitis -> asthma features with pANCA positive

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104
Q

What is the triangle of safety?

A
  • Located in the mid axillary line of the 5th intercostal space
  • Bordered by anterior edge of latissimus dorsi, lateral border of pectoralis major, line superior to the horizontal level of the nipple
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105
Q

Where is aspiration pneumonia most common?

A
  • Right middle and lower lobes
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106
Q

How is alpha 1 antitrypsin deficiency inherited?

A

Autosomal recessive

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107
Q

How can A1AD be managed?

A
  • Obstructive picture on spirometry
  • Supportive treatment with bronchodilators
  • Lung volume reduction surgery can be done in severe cases
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108
Q

Moderate asthma features

A

PEFR 50-75% best or predicted
Speech normal
RR < 25
Pulse < 110

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109
Q

Acute severe asthma features

A

PEFR 33-50% best or predicted
Can’t complete sentences
RR > 25
Pulse > 110

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110
Q

Life threatening asthma features

A

PEFR < 33% best or predicted
Sats <92%
Normal PCO2
Silent chest, cyanosis or poor resp effort
Bradycardia/Hypotension
Exhaustion/Confusion/Coma

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111
Q

What are some blood tests for sarcoidosis?

A
  • elevated ACE, ESR, calcium, immunoglobulins
  • Deranged LFTs
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112
Q

ECG signs of PE

A
  • Sinus tachycardia
  • Right BBB
  • S1 Q3 T3
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113
Q

Complications of recurrent or untreated PE?

A
  • Pulmonary HTN
  • Right sided heart failure
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114
Q

Surgical interventions for COPD?

A
  • Bullectomy
  • Lung reduction surgery
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115
Q

Extra-respiratory manifestations of cystic fibrosis

A
  • Pancreatic insufficiency
  • DM
  • Cirrhosis
  • Nasal polyps
  • Sinusitis
  • Male infertility
  • Osteoporosis
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116
Q

Over rapid aspiration/drainage of pneumothorax can result in what?

A

Reexpansion pulmonary oedema

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117
Q

What test should be offered to all patients with TB?

A

HIV

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118
Q

What size of pneumothorax would be indicated to do a needle aspiration?

A

> 2cm

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119
Q

Bilateral, mid-to-lower zone patchy consolidation in an older patient

A

Legionella

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120
Q

Deranged LFTs, hyponatraemia, low lymphocytes?

A

Legionella

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121
Q

Mycoplasma pneumonia can cause what?

A

Immune mediated neurological diseases e.g Guillan Barre

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122
Q

Pneumonia + red cell agglutination?

A

Mycoplasma

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123
Q

Large bullae in COPD can mimic what?

A

Pneumothorax

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124
Q

Why should intranasal decongestants not be used for prolonged periods?

A

Risk of tachyphylaxis -> increasing doses are needed

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125
Q

What is the Abx of choice for acute bronchitis?

A

Doxycycline

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126
Q

When to use NIV vs IV?

A

NIV - 7.25 - 7.35
IV - <7.25

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127
Q

What is used to assess drug sensitivities in TB?

A

Sputum culture

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128
Q

Staph aureus pneumonia is associated with what?

A

Cavitating lesions

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129
Q

What is the gold standard test for TB?

A

Sputum culture

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130
Q

HIV decreases what?

A

Sensitivity to sputum smear for TB

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131
Q

Investigation to diagnose mesothelioma?

A

Thoracoscopy with histology

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132
Q

Pneumonia with cold sores?

A

Strep pneumoniae

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133
Q

Marked volume loss of the lung with thickening of the pleura?

A

Think mesothelioma

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134
Q

What is the management of empyema?

A

Chest drain insertion for drainage + IV Abx

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135
Q

What is the advice around air travel following pneumothorax?

A

No travel until full resolution on CXR

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136
Q

Acute asthma steps

A
  • Oxygen
  • Nebulised salbutamol
  • Oral steroids
  • Nebulised Ipratropium
  • IV Mag Sulph
  • IV Aminophylline -> discuss with seniors
  • Intubation and Ventilation in HDU/ITU
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137
Q

What is criteria for discharge following asthma exacerbation?

A
  • Stable on discharge meds for 12-24 hours
  • Inhaler technique checked
  • PEFR > 75%
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138
Q

Asthma stepwise management for adults

A
  1. SABA
  2. SABA + ICS
  3. SABA + ICS + LTRA
  4. SABA + ICS + LABA (+LTRA if helping)
  5. SABA + MART (ICS+LABA) (+LTRA if helping)
  6. SABA + medium dose MART (+LTRA if helping)
  7. Seek help from secondary care
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139
Q

Asthma stepwise management for children

A
  1. SABA
  2. SABA + ICS
  3. SABA + ICS + LTRA
  4. SABA + ICS + LABA
  5. SABA + MART
  6. SABA + medium dose MART
  7. Seek help from secondary care
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140
Q

COPD stepwise medical Mx

A
  1. SABA or SAMA
  2. SABA + LABA + LAMA if no asthma features OR SABA + LABA + ICS if asthma features
  3. SABA + LAMA + LABA + ICS (even if no asthma features)
  4. Seek help from secondary care
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141
Q

What would chronic bronchitis COPD show on V/Q?

A

Low V/Q due to decreased ventilation

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142
Q

What would emphysema COPD show on V/Q?

A

High V/Q due to loss of alveolar surface area causing more ventilation per available perfusion area

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143
Q

CXR signs for COPD

A
  • Hyperinflated chest
  • Bullae (if large may mimic pneumothorax)
  • Decreased peripheral vascular markings
  • Flattened diaphragm
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144
Q

Where will pancoast tumours be?

A
  • Same side as the Horner’s signs
  • At the lung apex
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145
Q

Heart sounds

A

1st - mitral/tricuspid
2nd - aortic/pulmonary

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146
Q

Split second heart sound with loud pulmonary component?

A

Cor pulmonale

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147
Q

TB Treatment

A

RIPE - 2 months
RI - 4 more months

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148
Q

Management of secondary pneumothorax which is not improving post chest-drain insertion?

A

Discuss with cardiothoracic

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149
Q

Diffuse alveolar damage with hyaline membrane formation

A

Acute respiratory distress syndrome

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150
Q

Pleural effusions due to rheumatoid arthritis have what?

A

Low glucose levels

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151
Q

massive haemoptysis

A

Think lung abscess

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152
Q

What does a pancoast tumour invade when it causes Horners?

A

Cervical sympathetic plexus

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153
Q

bilateral pulmonary infiltrates

A

Think ARDS

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154
Q

Patient with swallowing difficulties/previous stroke with resp pathology?

A

Think lung abscess

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155
Q

What is the initial management of hypercalcaemia?

A

IV Fluids

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156
Q

What pharmacological therapy can be used for idiopathic pulmonary fibrosis?

A

Pirfenidone / Nintedanib

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157
Q

What is a pneumothorax?

A

Air in the pleural cavity which is the potential space between the visceral and parietal pleura

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158
Q

Where do you measure for pneumothorax?

A

Chest wall to the outer edge of the lung at level of hilum

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159
Q

What are surgical options for recurrent pneumothorax?

A

Video assisted thorascopic surgery
Surgical pleurodesis

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160
Q

PE like symptoms following a percutaneous vertebroplasty?

A

Pulmonary cement embolism

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161
Q

diffuse bilateral opacities on x ray?

A

Think ARDS

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162
Q

Management of solitary pulmonary nodules?

A

CT guided needle aspiration biopsy if >8mm

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163
Q

Unilateral pleural effusion?

A

Rule out malignancy

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164
Q

Why can people with carbon monoxide poisoning have?

A

Normal O2 sats as monitors cannot differentiate between the 2

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165
Q

Investigation of choice for pnemocystitis jiroveci?

A

Bronchoalveolar lavage

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166
Q

Acute bronchitis?

A

LRTI which causes inflam in bronchial airways causing oedematous large airways and sputum production.
Normally resolves in 3w but 25% will have cough after

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167
Q

Mx for acute bronchitis?

A
  • self-care: NSAIDs/paracetamol; honey; stop smoking; seek help if systemically unwell or don’t improve after 3-4w
  • Abx if indicated but not routine (only shortens cough by half a day and S/Es & resistance)
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168
Q

When to offer Abx for acute bronchitis?

A
  • Immediate= systemically unwell
  • Consider= high risk of Cx eg. CF, immunosupression, comorbid condition; >65yrs with 2 or >80yrs with 1: DM, hospital admission <1yr, CHF, take corticosteroids
  • Back-up prescription= if not needed but pick up if worse rapidly
  • CRP levels
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169
Q

When to offer Abx for acute bronchitis based on CRP levels?

A

CRP <20= not routine

CRP 20-100= consider delayed

CRP >100= Abx

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170
Q

Abx for acute bronchitis if indicated?

A

Oral doxycycline 200mg 1st day then 100mg OD for 4d

pregnant or 12-17yrs = amoxi 500mg 3xd 5d

or clarithro

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171
Q

Cause of acute bronchitis?

A

uncertain but likely virus; 80% cases in autumn/winter

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172
Q

CP of acute bronchitis?

A
  • cough: productive or not
  • sore throat
  • rhinorrhoea
  • may have wheeze
  • low grade fever
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173
Q

Differentiate acute bronchitis from pneumonia?

A

Hx= sputum, wheeze, breathlessness may be absent in AB but at least one present in P

Ex= no other focal chest signs (dullness to percussion, creps, bronchial breathing) in AB except wheeze. Systemic symptoms more likely in pneumonia (malaise, myalgia, fever)

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174
Q

Ix for acute bronchitis?

A

CLINICAL

  • CRP can be used to guide if Abx therapy indicated
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175
Q

Who can not take doxycycline?

A

children or pregnant women, use amoxicillin instead

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176
Q

Allergic rhinitis?

A

inflam disorder of nose that occurs when nasal mucosa becomes exposed and sensitised to allergens, to produce typical symptoms of sneezing, nasal itching, rhinorrhoea and congestion

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177
Q

What type of inflam reaction is allergic rhinitis?

A

IgE mediated

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178
Q

Classification of allergic rhinitis?

A

Mild or moderate to severe or..

  • seasonal eg. grass, pollen (hayfever), around same time every yr
  • perennial (throughout yr) eg. dust mites, animals
  • intermittent= <4d a w or <4 consecutive w
  • persistent= >4d a w AND >4 consecutive w
  • occupations (allergens in work environment)
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179
Q

When does allergic rhinitis usually begin?

A

childhood/adolescence

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180
Q

Cx of allergic rhinitis?

A

reduced QOL, impaired school/work performance, disturbed sleep, reduced conc, possible development of: asthma, sinusitis, nasal polyps

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181
Q

Features of allergic rhinitis?

A
  • occurs after exposure to known causative allergen
  • sneeze, nasal itch, rhinorrhoea, congestion, post-nasal drup
  • associations: allergic conjunctivitis, asthma, eczema
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182
Q

Mx for allergic rhinitis?

A
  • ?saline nasal irrigation
  • allergen avoidance
  • prn intranasal antihistamine or non-sedating oral
  • regular intranasal corticosteroids during allergen exposure for moderate to severe or if inital Mx ineffective
  • review 2-4w if persist
  • refractory= intranasal antihis + corticosteroid spray
  • ? add on eg. short course intranasal decongestant, intranasal anticholinergic or LTRA
  • severe uncontrolled: short course oral corticosteroids
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183
Q

When to refer to allergy or ENT for allergic rhinitis?

A
  • Red flags
  • unresponsive to Mx
  • allergy testing may be needed if think its house dust mite or animal
  • uncertain
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184
Q

Why should nasal decongestants eg. oxymetazoline not be used for prolonged periods?

A

Increasing doses will be needed to achieve same effect (tachyphylaxis) and rebound hypertrophy of nasal mucosa (rhinitis medicamentosa) may occur upon withdrawl

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185
Q

Types of allergy tests?

A
  • skin prick
  • Radioallergosorbent test (RAST)
  • skin patch
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186
Q

Skin prick allergy test?

A
  • most common
  • drops of diluted allergen placed on skin after which the skin in pierced with needle
  • large no. allergens can be tested in 1 session
  • Normally incl. histamine (+ve) and sterile water (-ve control)
  • a wheal will typically develop if pt has allergy after 15minds
  • good for food allergy and pollen
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187
Q

Radioallergosorbent test for allergy?

A
  • determines amount of IgE that reacts with suspected or known allergens eg. IgE to egg protein
  • results given in grades: 0 (-ve) to 6 (strongly +ve)
  • good for food allergies, inhaled allergens (eg. pollen) and wasp/bee venom
  • when skin prick not suitable eg. extensive eczema or pt taking antihistamines
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188
Q

Skin patch allergy testing?

A
  • useful for contact dermatitis
  • 30-40 allergens placed on back
  • irritants may also be tested for
  • patches are moved 48hrs later with results being read by derm after further 48hrs
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189
Q

Food allergy describes what?

A

adverse immune-mediated response which occurs when person is exposed to specific food allergen(s).

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190
Q

IgE mediated food allergy produces what?

A

immediate and consistently reproducible multi-organ symptoms

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191
Q

Common food allergies?

A

cow’s milk, eggs, peanuts and other legumes, tree nuts, shellfish, fish and wheat

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192
Q

RFs for development of food allergy?

A

pre-existing food allergy, atopic eczema, FHx food allergy and/or atopy

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193
Q

Possible Cx of food allergy?

A
  • severe/life-threatening rections (incl. anaphylaxis)
  • anxiety
  • reduced QOL (restrictions, social interactions, peer pressure, stigma, embarrassment, social exclusion)
  • restricted diet and malnutrition
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194
Q

When should diagnosis of IgE mediated food allergy be suspected?

A

classic symptoms develop within secs or mins to 1-2hrs after ingestion of trigger food:
- urticaria
- angioedema
- itching
- cough
- hoarseness
- wheeze
- SOB
- N & V
- diarrhoea
- abdo pain

consider if unexplained persistent symptoms of atopic eczema

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195
Q

Assessment of suspected IgE mediated food allergy?

A
  • examine nutritional status and signs of clinical reaction/comorbid conditons + Hx
  • arrange skin prick testing and/or serum-specific IgE allergy testing
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196
Q

Referral for pt with food allergy?

A
  • A&E= systemic symptoms or ?anaphylaxis
  • allergy specialist= multiple; uncertain; signif atopic eczema; Hx of systemic symptoms or increased risk anaphylaxis; persistent food allergy
  • Dietician= nutritional concerns or already on restricted diet
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197
Q

Mx of food allergy?

A
  • individualised written allergy Mx plan
  • advise on prompt recognition and Mx of acute symptoms= immediate oral antihistamines (cetirizine or chlorphenamine if <2yrs) for non-severe symptoms or adrenaline auto-injector for suspected anaphylaxis
  • review annually
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198
Q

Systemic symptoms of food allergy that suggest anaphylaxis?

A

resp distress; wheeze; hypotension; tachy or bradycradia; drowsiness; confusion; collapse; loss of consciousness

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199
Q

Differential diagnosis for IgE-mediated food allergy?

A
  • acute spontaneous urticaria and angioedema (no allergic trigger, often following viral infection)
  • carcinoid syndrome
  • food intolerance (non-immune, non-specific reactions, delay in CP and prolonged symptoms)
  • food poisoning and toxic reactions
  • food aversion or refusal
  • IBS/IBD
  • urticaria
  • asthma exacerbation
  • atopic dermatitis
  • coeliac
  • GORD
  • gastroenteritis
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200
Q

Mx of IgE mediated allergy vs non-IgE mediated?

A

IgE= skin prick or bloods specific for IgE antibodies

Non-IgE= eliminate suspected allergen for 2-6w then introduce; consult dietician about nutritional adequancies, timing and follow up

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201
Q

IgE-mediated food allergy vs Non-IgE mediated presentation?

A

IgE:
- anaphylaxis
- skin= pruritus, erythema, urticaria, angioedema
- GI= N, V, D, colicky abdo pain
- Resp= URT symptoms (nasal itching, sneezing, rhinorrhoea, congestion); LRT symptoms (cough, wheeze, chest tightness, SOB)

Non-IgE:
- skin= pruritus, erythema, atopic eczema
- GI= GORD; loose/frequent stool; blood/mucus in stool; abdo pain; infantile colic; food refusal or aversion; contipation; perianal redness; pallor/tired; faltering growth + other symptoms above

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202
Q

Sensitivity to latex may cause what problems?

A
  • type I hypersensitivity (anaphylaxis)
  • type IV hypersensitivity (allergic contact dermatitis)
  • irritant contact dermatitis
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203
Q

Latex allergy is more common in who?

A

children with myelomeningocele spina bifida

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204
Q

Latex-fruit syndrome?

A

people who are allergic to latex are also allergic to fruits, particularly: banana, avocado, pineapple, kiwi, chestnut, mango, passion fruit, strawberry

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205
Q

Oral allergy syndrome?

A

aka pollen-food allergy

IgE mediated hypersensitivity reaction to specific raw, plant-based foods incl. fruits, vegetables, nuts and certain spices.

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206
Q

How does oral allergy syndrome (pollen-food allergy) typically present?

A

mild tingling or pruritus of lips, tongue and mouth

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207
Q

How is the hypersensitivity reaction in oral allergy syndrome initiated?

A

by cross-reaction with non-food allergen, most commonly birch pollen whereby the protein in food is similar but not identical in structure to original allergen (explains why OAS strongly linked with pollen allergies & why cooking culprit food prevents symptoms-denatures the protiens)

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208
Q

What is oral allergy syndrome (OAS) strongly linked with?

A

pollen allergies and seasonal variation

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209
Q

What can you do to prevent symptoms occurring in oral allergy syndrome?

A

cooking culprit food- denatures the proteins

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210
Q

OAS vs food allergy?

A
  • food allergy= direct sensitivity to a protein present in food. OAS= cross-sensitisation to a structurally similar allergen present in pollen
  • food allergens can be caused by plant or non-plant foods but OAS is not caused by non-plant foods
  • OAS normally limited to oropharynx but food allergies more likely to cause systemic symptoms (V&D)
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211
Q

Why do non-plant foods not cause OAS but food allergies can be caused by plant and non-plant foods?

A

OAS= no cross-reactive allergens in pollen which would be structurally similar to meat

Food allergy= allergens occur in response to substances that are more stable and able to survive stomach enzymes and acid processing and cooking

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212
Q

Why are food allergies more likely to cause systemic symptoms (eg. V&D) but OAS is limited to oropharynx?

A

Food allergy= allergens are not readily broken down

OAS= proteins that cause the symptoms are denatured by stomach enzymes

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213
Q

About 1/2 of pts with general pollen allergy and 3/4 pts with allergy to birch pollen (most common allergen in UK) report symptoms of what?

A

OAS

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214
Q

Associations with OAS?

A
  • birch pollen allergy (most common)
  • Rye grass pollen allergy
  • Rubber latex allergy
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215
Q

Presentation of OAS?

A
  • suspect in pts with Hx of seasonal allergy symptoms and present with symptoms mins after eating a specific raw food
  • itching, tingling of lips, tongue and mouth
  • mild swelling and redness of lips, tongue and throat may occur
  • severe= N&V
  • fully resolve within 1hr of contact
  • anaphylaxis very rare
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216
Q

Ix for OAS?

A
  • clinical but can use allergy testing to rule out food allergies if Hx unclear
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217
Q

Mx for OAS?

A
  • avoid culprit foods
  • can take oral antihistamine if get symptoms
  • inform that once cooked it shouldn’t cause symptoms
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218
Q

Many pts who report an allergy to penicillin may be describing what?

A

intolerance/side efects eg. diarrhoea or a coinincidental rash eg. amoxicillin in pts with infectious mononucleosis

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219
Q

0.5-6.5% of pts who are allergic to penicillin are also allergic to what?

A

cephalosporins

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220
Q

Pts with Hx of immediate hypersensitivity to penicillin should not receive a what? What if it is essential because an alternative Abx is not available?

A

Cephalosporin.

If pt needs cephalosporin then can use: cefixime, cefotaxime, ceftazidime, ceftriaxone or cefuroxime with caution.
AVOID= cefaclor, cefadroxil, cefalexin, cefradine and ceftaroline fosamil

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221
Q

Types of penicillin? (to be aware of to avoid accidental prescription if pt has allergy)

A
  • phenoxymethylpenicillin
  • benzylpenicillin
  • flucloxacillin
  • amoxicillin
  • ampicillin
  • co-amoxiclave (Augmentin)
  • co-fluampicil (Magnapen)
  • piperacillin with tazobactam (Tazocin)
  • ticarcillin with clavulanic acid (Timentin)
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222
Q

Allergic reactions to venom eg. after insect bite/sting may be considered as long or systemic, what does this mean?

A
  • Local= redness, swelling, pain limited to skin and soft tissues directly related to the site of venom exposure but spreading >10cm from the site
  • Systemic= cutaneous reactions that are relatively distant from the exposure site eg. widespread redness, itching, urticaria and/or angioedema (not affecting mouth or throat)

Anaphylaxis may occur with/without evidence of systemic cutaneous reaction & any reaction there is any airway compromise or signs of haemodynamic compromise should be managed as anaphylactic in nature

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223
Q

Mx of venom allergy eg. after insect bite or sting?

A

Supportive: remove stingers by scraping sideways with fingernail or card; cold compress; avoidance of scratching to prevent secondary infection.

Can use oral paracetamol/ibuprofen for pain, topical hydorcortisone and oral antihistamines eg. chlorphenamine to reduce itching.

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224
Q

When should referral to an allergy specialist be made for pt with venom allergy (insect bite or sting)?

A

if pt has had or suspected of having a systemic reaction

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225
Q

Testing for venom allergy is recommended in who?

A

pt with a history of systemic reaction causing airway compromise or haemodynamic instability

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226
Q

Mx for pt with history of previous reaction to insect bite/sting which presented with airway and/or haemodynamic compromise and raised levels of venom-specific IgE on skin prick or in vitro testing?

A

Venom immunotherapy (VIT)

Baseline tryptase level should be preformed to exclude indolent mastocytosis or monoclonal mast cell activation syndrome

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227
Q

What can asbestos cause in the lung?

A
  • Pleural plaques
  • Pleural thickening
  • Asbestosis
  • Mesothelioma
  • Lung cancer
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228
Q

What are pleural plaques (can be caused by asbestos)?

A

benign and do NOT undergo malignant change
- don’t require follow uo
- most common form of asbestos related lung disease
- occur after a latent period of 20-40yrs

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229
Q

What is pleural thickening (can be caused by asbestos)?

A

asbestos exposure can cause diffuse pleural thickening in similar pattern seen following an empyema or haemothorax

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230
Q

What is asbestosis (can be caused by asbestos)?

A
  • Typically causes lower love fibrosis
  • severity linked to length of exposure (contrast to mesothelioma- limited exposure can cause disease)
  • Patent period 15-30yrs
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231
Q

Features of asbestosis?

A
  • SOB & reduced exercise tolerance
  • clubbing
  • bilateral end-inspiratory crackles
  • restrictive pattern with reduced gas transfer on lung function tests
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232
Q

What do lung function tests show for asbestosis?

A

restrictive pattern with reduced gas transfer

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233
Q

Treatment for asbestosis?

A

conservative as no interventions offer signif benefit

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234
Q

What is mesothelioma?

A

Cancer of the mesothelial layer of the pleural cavity that is strongly associated with asbestos exposure (other m. layers may be affected eg. abdo in small no. of cases).

  • Latent period= 30-40yrs
  • Even very limited exposure to asbestos can cause it
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235
Q

Most dangerous form of mesothelioma?

A

Crocidolite (blue) asbestos

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236
Q

Possible features of mesothelioma?

A
  • progressive SOB
  • chest wall pain
  • painless pleural effusion (30%)
  • 20% have pre-existing asbestosis
  • weight loss
  • clubbing
  • 85-90% have Hx of asbestos exposure
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237
Q

Mx for mesothelioma?

A
  • palliative chemo, surgery if operable
  • industrial compensation
  • prognosis v. poor= median survival from diagnosis of 8-14m
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238
Q

Most common form of cancer associated with asbestos exposure?

A

LUNG cancer most common

Mesothelioma also associated but less common

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239
Q

What is important for pt to do if they smoke and have a history of asbestos exposure?

A

smoking cessation as the risk of lung ca in smokers who have history of asbestos exposure is very high

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240
Q

Overview of the malignancy in mesothelioma?

A
  • malignancy of mesothelial cells of pleura
  • mets to contralateral lung and peritoneum
  • R lung affected more than L
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241
Q

Ix and diagnosis for mesothelioma?

A
  • CXR shows pleural effusion or pleural thickening
  • get pleural CT= if area of pleural nodularity seen then image-guided pleural biopsy
  • pleural effusion present= send fluid for MC&S, biochemistry and cytology
  • cytology -ve exudative effusion= local anaesthetic thoracoscopy

DIAGNOSIS= histology following thoracoscopy

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242
Q

Asthma?

A

chronic inflam condition of the airways: airways are hyper-responsive and constrict easily in response to wide range of stimuli. May result in coughing, wheezing, chest tifhtness and SOB.

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243
Q

Suspect asthma in who (CP)?

A
  • wheeze, breathlessness, chest tightness, cough
  • Diurnal= worse at night and early morning
  • occur in response to exercise, allergen exposure, cold air; occur after taking NSAIDs, BB; occur in absence of URTI
  • Hx of atopic disorder
  • Widespread bilateral polyphonic expiratory wheeze
  • may be triggered by emotion and laughing in children
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244
Q

Ix that help support asthma diagnosis (not one single diagnostic test)?

A
  • Fractional exhaled nitric oxide (FeNO) testing (sometimes primary care but may require referal). (ALL)
  • Spirometry (all symptomatic pts >5yrs) then do Spirometry with bronchodilator reseversibility (BDR). (ALL).
  • Peak expiratory flow (can do in ALL or if uncertain)
  • direct bronchial challenge testing with histamine or methocholine (specialist referal needed) (if uncertain/negative results)
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245
Q

FeNO test for asthma?

A

in steroid naive adults…

+ve if 40ppb or higher (adults) or 35 in children (only do in children in uncertain after spirometry)

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246
Q

Spirometry test for asthma?

A

all symptomatic pts >5yrs (FeV1/FVC <70% is +ve result and suggest airflow obstruction).

THEN DO:

  • Spirometry with bronchodilator reversibility (BDR): adults= improvement of 12%+ with increased volume of 200mL+ in response to SABA or corticosteroids is positive for asthma. Improvement >400mL in FEV1 is strongly suggestive. Children= improvement of FEV1 of 12%+ is positive.
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247
Q

Peak expiratory flow test for asthma?

A

Value of >20% variability after monitoring at least twice daily for 2-4w if positive for asthma. PEF variability calculated: difference between highest and lowest readings expressed as a % of the average PEF. Upper limit of normal is approx 20% using at lest PEF reading per day but may be lower when using twice daily readings.

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248
Q

Direct bronchial challenge testing with histamine or methocholine (specialist referal needed) for asthma?

A

PC20 value of 8mg/ml or less is positive. Offer if normal spirometry and FeNO of 40 but no variability in PEF or FeNO <40 but with variablility in PEF

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249
Q

When to diagnose, suspect or consider alternative diagnosis/refer for specialist opinion in asthma?

A
  • DIAGNOSE= FeNO level 40ppb+ with either +ve BDR, +ve PEFV or bronchial hyperactivity. OR + BDR AND +ve PEFV irrespective of FeNO level.
  • SUSPECT= obstructive spirometry with: -ve BDR, FeNO level 40+ or FeNO level 25-39 but with +ve PEFV
  • alternative diagnosis/specialisgt if normal spirometry, FeNO and PEFV
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250
Q

What if suspect asthma in pt <5yrs?

A

use CP to determine likelihood and when reach 5 carry out the objective tests

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251
Q

Asthma Mx in adults (17yrs+)?

A

1) SABA

2) SABA + low dose ICS

3) SABA + ICS + LTRA

4) SABA + ICS + LABA (+ LTRA if good response to LTRA)

5) SABA + MART with lose dose ICS (+/- LTRA)

6) SABA + MART with moderate dose ICS
notion

7) SABA + MART with high dose ICS OR trial additional drug eg. LAMA

8) specialist referral

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252
Q

Asthma Mx in pts aged 5-16yrs?

A

1) SABA

2) SABA + lose dose ICS

3) SABA + ICS + LTRA

4) SABA + ICS + LABA

5) SABA + MART with lose dose ICS

6) SABA + MART with moderate dose ICS

7) specialist referral

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253
Q

Asthma Mx for children <5yrs?

A

1) SABA

2) SABA + 8w trial of moderate dose ICS

3) after 8w stop ICS and monitor symptoms.
- if didn’t resolve during trial= alternative diagnosis
- if resolved but then reoccured within 4w stopping ICS= restart ICS at lose dose
- if resolved but reoccured >4w after stopping ICS= repeated 8w trial of moderate dose ICS

4) SABA + low dose ICS + LTRA

5) stop LTRA and specialist referral

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254
Q

When to refer to resp for pt with asthma?

A

if symptoms not controlled after all Mx steps, lower threshold for children

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255
Q

Follow up for asthma?

A

annual

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256
Q

FeNO testing in asthma can be effected by what?

A

inhaled corticosteroids
approx 1 in 5 with -ve result will have asthma
approx 1 in 5 with +ve result won’t have asthma

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257
Q

Red flags that suggest an alternative diagnosis to asthma and prompt immediate resp referral?

A

Adults= systemic features (myalgia, fever, weight loss); non-variable SOB; unexpected clincial signs (crackles, clubbing, cyanosis, cardiac disease, monophonic wheeze, stridor); chronic sputum; CXR shadowing; unexplained restricted spirometry; blood eosinophilia

Children= FTT; focal signs, abdnorm voice/cry, dysphagia, inspiratory stridor; symptoms present from birth; XS vomiting/posseting; severe URTI; persistent wet productive cough; FHx unusual chest disease; nasal polyps

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258
Q

Obstructive vs restrictive spirometry?

A

Obstructive:
- eg. asthma, COPD, bronchitis
- FEV1 decreased
- FVC normal or decreased
- FEV1/FVC ratio= <70%

Restrictive:
- eg. sarcoidosis, pulmonary fibrosis, interstitial lung disease, (conditions affecting chest wall, muscles or pleura)
- FEV1 decreased
- FVC decreased
FEV1/FVC= >=70%

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259
Q

Spirometry: FEV1 vs FVC?

A

FEV1= forced expiratory volume in 1 sec
FVC= forced vital capacity

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260
Q

How is complete control of asthma defined?

A
  • no daytime symptoms
  • no night waking due to asthma
  • no need for rescue meds (SABA)
  • no asthma attacks
  • no limitations on activity incl exercise
  • normal lung function (PEF >80% predicted or best)
  • minimal side effects from meds
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261
Q

Advice for pt with asthma?

A
  • keep up to date with routine vaccinations incl. annual flu
  • avoid triggers
  • weight loss and smoking cessation
  • assess for anxiety/depression
  • ensure pt has own peak flow meter
  • explain how to use inhaler incl if using a spacer (can use tidal breathing, washed and dry in air)
  • SABA for reliever therapy and ICS for preventer
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262
Q

Asthma MX: lose dose ICS?

A

400ug (micrograms) budesonide

if =<16yrs= 200ug

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263
Q

Asthma Mx: moderate dose ICS?

A

400-800ug budesonide

=<16yrs= 200-400ug

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264
Q

Asthma Mx: high dose ICS?

A

> 800ug budesonide

=<16yrs= >400ug

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265
Q

Asthma Mx: MART?

A

Maintenance and reliever therapy.
Form of combined ICS and fasting-acting LABA in a single inhaler.

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266
Q

When could you consider decreasing maintenance therapy for pts asthma?

A

once it has been controlled with their current maintenance therapy for at least 3m.

decrease ICS dose slow: every 3m by 25-50%

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267
Q

Monitoring pts for asthma?

A

Annually
But review response to Mx after 4-8w

  • spirometry or peak flow
  • advice on inhaler technique
  • no. of attacks, ICS use, time off school/work due to asthma; nocturnal symptoms; adherence; hospital admissions
  • use of SABA (overuse= >12 per hr)

If on long term steroid (>3m) then monitor= BP; HbA1c; cholesterol; BMD; vision

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268
Q

3 questions to ask every pt with asthma?

A

Have you had difficulty sleeping because of your asthma symptoms (including cough)?

Have you had your usual asthma symptoms during the day (e.g. cough, wheeze, chest tightness, or breathlessness)?

Has your asthma interfered with your usual activities (e.g. housework, work, school)?

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269
Q

Asthma Mx: SABA?

A

Short-acting beta-2 agonists

eg. salbutmol

rapid onset (<5mins) and last up to 4hrs

up to 4x a day (not exceding 4hrly)

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270
Q

Asthma Mx: LABA?

A

Long-acting beta-2 agonists

eg. salmeterol

last 12hrs

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271
Q

What drugs should pts with asthma avoid?

A

NSAIDs
Beta-blockers

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272
Q

Adverse effects of beta-2 agonists (SABA & LABA)

A
  • fine tremor: hands, worse in 1st few days of Mx
  • palpitations
  • headache
  • seizure
  • hypokalaemia
  • anxiety
  • cardiac arrhythmia and paradoxoical bronchospasm (rare)
  • acute angle-closure glaucoma
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273
Q

Use beta-2 agonists eg. SABA & LABA with caution in who?

A
  • hyperthyroidism (may stimulate T activity)
  • DM (rare risk ketoacidosis)
  • CVD & HTN
  • QT-prolongation
  • hypokalaemia
  • convulsive disorders
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274
Q

Asthma Mx: LTRA?

A

leukotriene receptor antagonist

eg. montelukast 10mg OD in evening

5-16yrs= 5mg
<5yrs= 4mg

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275
Q

What pts need hospital admission for acute exacerbation of asthma?

A
  • all life-threatening
  • severe which persists after initial bronchodilator Mx
  • moderate with worsening symptoms despite BD Mx and/or had previous near fatal attack in past. Or if: <18yrs; poor treatment adherence; live alone; recent hospital admission; previous severe attack
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276
Q

Mx for acute exacerbation of asthma whilst awaiting admission to hospital?

A

1) supp O2 if hypoxia to maintain sats 94-98%

AND

2) severe= NEBULISED SALBUTAMOL (5mg) oxygen driven (flow rate 6L/min) over 30-60mins.
2) moderate= pressurised metered-dose inhaler with large volume spacer; 4 piuffs then 2 puffs every 2mins up to 10 puffs; can repeat every 10-20mins. (children-puff every 30-60secs up to 10puffs)

AND if severe/poor response

3) NEBULISED IPRATROPIUM BROMIDE (500ug adults, 250ug children). Do not repeat within 4hrs.

AND

4) give 1st dose of PREDNISOLONE (40-50mg adults, 30-40mg >5yrs, 20mg <5) ; if can’t swallow then IV hydrocortisone 100mg

AND

5) monitor PEF and O2 sats to assess response to Mx

6) short course oral pred

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277
Q

Mx for acute exacerbation of asthma if pt does not need hospital admission?

A

1) SABA via large volume spacer

AND

2) Adults= short course oral prednisolone

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278
Q

Acute exacerbation of asthma follow up?

A

within 48hrs if not admitted to hospital; or within 48hrs of discharge

  • PEF and review CP
  • check inhaler technique
  • consider stepping up Mx
  • advice on recognising poor asthma control and early signs of exacerbation (sudden persistent worsening symptoms)
  • give oral corticosteroids to take if have early signs of exacerbation
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279
Q

When to consider referral to resp for asthma after acute exacerbation?

A

2 asthma attacks within 12m

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280
Q

Summary of Mx for acute exacerbation of asthma if pt is admitted to hospital and attack is severe/life-threatening?

A

1) NEBULISED SALBUTAMOL (5mg) oxygen driven (flow rate 6L/min) over 30-60mins.

AND

2) NEBULISED IPRATROPIUM BROMIDE (500ug adults, 250ug children)

AND

3) 1st dose of PREDNISOLONE (40-50mg adults, 30-40mg >5yrs, 20mg <5) ; if can’t swallow then IV hydrocortisone 100mg

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281
Q

How long should pt take oral pred after acute exacerbation of asthma?

A

5d

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282
Q

Moderate attack of asthma in children 2-5yrs?

A

SpO2 > 92%
No clinical features of severe asthma

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283
Q

Severe attack of asthma in children 2-5yrs?

A

SpO2 < 92%
Too breathless to talk or feed
Heart rate > 140/min
Respiratory rate > 40/min
Use of accessory neck muscles

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284
Q

Life-threatening attack of asthma in children 2-5yrs?

A

SpO2 <92%
Silent chest
Poor respiratory effort
Agitation
Altered consciousness
Cyanosis

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285
Q

Moderate attack of asthma in children >5yrs?

A

SpO2 > 92%
PEF > 50% best or predicted
No clinical features of
severe asthma

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286
Q

Severe attack of asthma in children >5yrs?

A

SpO2 < 92%
PEF 33-50% best or predicted
Can’t complete sentences in one breath or too breathless to talk or feed
Heart rate > 125/min
Respiratory rate > 30/min
Use of accessory neck muscles

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287
Q

Life-threatening attack of asthma in children >5yrs?

A

SpO2 < 92%
PEF < 33% best or predicted
Silent chest
Poor respiratory effort
Altered consciousness
Cyanosis

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288
Q

Normal pCO2 in acute asthma attack?

A

indicates exhaustion and should be classified as life-threatening

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289
Q

Near-fatal asthma?

A

Raised pCO2 and/or requiring mechanical ventilation with raised inflation pressures

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290
Q

Mx for pts who fail to respond to any intervention for acute asthma attack?

A

admit ITU/HDU for intubation and ventilation

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291
Q

Criteria for discharge after acute asthma exacerbation?

A
  • been stable on their discharge medication (i.e. no nebulisers or oxygen) for 12-24 hours
  • inhaler technique checked and recorded
  • PEF >75% of best or predicted
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292
Q

When diagnosing asthma, what tests should all pts have?

A

Adults:
- spirometry with BDR
- FeNO test

5-16yrs:
- spirometry with BDR
- FeNO if normal S or obstructive S with -ve BDR

<5yrs:
- clinical

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293
Q

Asthma-COPD overlap syndrome (ACOS)?

A

pts with airway disease who have features of both asthma and COPD

10-30% of asthma and COPD pts

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294
Q

Criteria for asthma-COPD overlap syndrome?

A
  • > 40yrs
  • resp symptoms (eg. exertional dyspnoea) persistent but variability in symptoms may be prominent
  • persistent airflow obstruction
  • Hx of asthma or evidence of partial BDR
  • exposure to a RF eg. >=10 pack yr tabacco smoking or equivalent indoor/outdoor air pollution
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295
Q

Pathophysiology of asthma-COPD overlap syndrome?

A
  • Asthma= eosinophilic inflam, reversible airway obstruction and airway hyperresponsiveness
  • COPD= neutrophilic inflam, irreversible airway obstruction and progressive airflow limitation due to alveolar destruction (emphysema) and chronic bronchitis
  • ACOS= combination of both so more complex disease process
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296
Q

Mx for ACOS?

A
  • smoking cessation, immunisation, inhaler technique
  • SABA for symptomatic control
    + ICS (low or moderate)
  • can + LABA or LAMA

need specialist input as more exacerbations, lower QOL and decline in lung function and mortality worse in ACOS than just asthma or COPD

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297
Q

Bronchiectasis?

A

Persistent or progressive chronic debilitating disease characterised by permanent dilation of the bronchi due to irreversible damage to elastic and muscular components of the bronchial wall

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298
Q

What is bronchiectasis caused by?

A

inflam damage to airways:
irreversible damage to elastic and muscular components of bronchial wall causing permanent dilation of the bronchi

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299
Q

Clinical features of bronchiectasis?

A
  • daily expectoration of large volumes of purulent sputum
  • cough
  • SOB
  • haemoptysis
  • non-pleuritic chest pain between exacerbations
  • coarse crackles during early inspiration
  • wheeze
  • high pitched inspir squeaks
  • large airway rhonchi (low pitched sore like sound)
  • palpable chest secretions on coughing
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300
Q

Suspect bronchiectasis in adults with what?

A
  • cough >8w with sputum production or Hx of trigger
  • RA + chronic productive cough or recurrent chest infections
  • COPD with 2+ exacerbations annually and/or +ve sputum culture for Pseudomonas aeruginosa whilst stable
  • IBD + chronic productive cough
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301
Q

Suspect bronchiectasis in children with what?

A
  • chronic productive cough unresponsive to 4w Abx, between viral colds or with +ve sputum culture for = s. aureus, H. influenza, P.aeruginosa, non-TB mycobacteria or Burkholderia capacia complex
  • wet wough >6w
  • asthma unresponsive to Mx
  • severe pneumonia where symptoms, signs or radiological changes don’t complete resolve
  • recurrent pneumonia
  • localised chronic bronchial obstruction
  • exertional SOB
  • unexplained haemoptysis
  • persistent & unexplained signs or CXR abnormalities
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302
Q

Ix for bronchiectasis?

A
  • sputum culture
  • CXR
  • spirometry
  • O2 sats
  • and FBC incl WCC
  • refer to resp to confirm diagnosis
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303
Q

Mx for infective exacerbation of bronchiectasis? (most in primary care but sometimes hospital admission may be needed)

A
  • previous microbio cultures should guide Abx therapy
  • if not available then local protocols, if not available then amoxicillin or clarithromycin/erythromycin
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304
Q

Signs on examination in bronchiectasis?

A
  • Coarse crackles, especially in the lower lung zones.
  • Wheeze.
  • High-pitched inspiratory squeaks.
  • Large airway rhonchi (low pitched snore-like sounds).
  • Palpable chest secretions on coughing or forced expiratory manoeuvre, persisting over time.
  • Finger clubbing (uncommon).
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305
Q

Clinical symptoms of bronchiectasis?

A
  • Daily expectoration of large volumes of purulent sputum
  • Dyspnoea
  • Fever
  • Fatigue, reduced exercise tolerance.
  • Haemoptysis that can be frank (up to 10 mL) or massive (more than 235 mL) (26–51.2%).
  • Rhinosinusitis.
  • Weight loss.
  • Chest pain that is present between exacerbations and is usually non-pleuritic
  • Sputum colonization with P. aeruginosa.
  • Young age at presentation.
  • History of symptoms over many years.
  • Absence of smoking history.
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306
Q

Differential diagnosis of bronchiectasis?

A
  • asthma
  • COPD
  • chronic sinusitis
  • pneumonia
  • lung ca
  • interstitial lung disease (asbestosis, hypersensitivity pneumonitis, pulmonary fibrosis, sarcoidosis)
  • TB
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307
Q

When to suspect an infective exacerbation in pt with bronchiectasis?

A
  • change in 1+ symptoms: increased sputum vol or purulence, worse SOB, increased cough or fatigue/malaise
  • new symptoms eg. fever, pleuritic pain or haemoptysis
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308
Q

Ix in secondary care for bronchiectasis?

A
  • high-resolution computed tomography (HRCT)= most frequently used to diagnose
  • test for CF
  • screen for gross antibody def eg. IgG, IgA, IgM= for all pts with confirmed diagnosis
  • serum total IgE and specific IgE/skin prick test to Aspergillus (exclude allergic bronchopulmonary aspergillosis)
  • specific antibody levels against strep pneumonia

could do= RF, anti-CCP, ANA and ANCA; HIV serology; A1AT def

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309
Q

What pts with bronchiectasis to be followed up in secondary care?

A

all to diagnose then

either follow up in primary care or

follow up in secondary care if:
- 3+ exacerbations in 1 yr
- chronic p.aeruginosa, MRSA or non-TB mycobacteria colonisation
- deteriorating or advanced disease
- allergic pulmonary aspergillosis
- long term Abx therapy
- associated RA, immune def, IBD, or primary ciliary dyskinesia
- considering lung transplant

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310
Q

Follow up for bronchiectasis?

A
  • Baseline severity score= Bronchiectasis Severity Index
  • Offer pulmonary rehab
  • BMI
  • check exacerbation Hx (refer for ?long-term prophy Abx if 3+ in 1yrs)
  • sputum sample and culture (refer if chronic colonisation for p.a, mycobacteria or MRSA)
  • MEDICAL RESEARCH COUNCIL DYSPNOEA SCALE
  • spirometry
  • O2 sats
  • sputum clearance exercises compliance (refer to physio if havent been taught)
  • Immunisation against influenza and strep pneumonia
  • tell pt how to recognise exacerbations and what to do if get one
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311
Q

Arrange hospital admission for pt with bronchiectasis and?

A
  • so unwell that need IV Abx (eg. cardioresp failure or sepsis)= cyanosis, confusion, marked SOB, rapid resps or laboured, peripheral oedema, 38C+
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312
Q

Mx for infective exacerbation of bronchiectasis if don’t need hospital admission?

A
  • sputum for C&S before starting Abx but don’t wait for results
  • Empirical Abx 7-14d (if already taking then stop and prescribe from different class)
  • airway clearance technique
  • Review Abx response once C&S available
  • Offer a LABA but NOT ICS
  • consider prophylactic Abx
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313
Q

Empirical Abx for acute exacerbation of bronchiectasis?

A
  • amoxicillin 500mg 3td for 7-14d
    or clarithromycin 500mg 2tds 7-14d
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314
Q

Prophylactic Abx for bronchiectasis if needed?

A

1st= azithromycin 500mg 3 times a week

min 6m but can use up to 1yr

If current P.aeruginosa= inhaled colistin

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315
Q

What should be done before starting pt on oral macrolides eg. azithromycin prophylaxis for bronchiectasis exacerbation?

A
  • ECG: assess QT interval
  • baseline LFTs
  • baseline exacerbation rate
  • microbio testing of sputum before starting
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316
Q

What should you do after starting pt on oral macrolides?

A
  • LFTs 1m and then every 6m after starting
  • ECG 1m after starting: if new QT prolongation then stop
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317
Q

What can cause bronchiectasis?

A
  • Post-infective= TB, measles, pertussis, pneumonia
  • CF
  • bronchial obstruction eg. lung ca, forign body
  • immune def: selective IgA, hypogammaglobulinaemia
  • allergic bronchopulmonary aspergillosis (ABPA)
  • ciliary dyskinetic syndromes: Kartagener’s, Young’s
  • yellow nail syndrome
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318
Q

Summary of 3 features and 3 signs of bronchiectasis?

A

Features:
- persistent productive cough, large vol of sputum may be expectorated
- dyspnoea
- haemoptysis

Signs:
- abnormal chest auscultation= coarse crackles; wheeze
- clubbing may be present

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319
Q

Most common organisms isolated from pts with bronchiectasis?

A
  • Haemophilus influenzae (most common)
  • Pseudomonas aeruginosa
  • Klebsiella spp.
  • Streptococcus pneumoniae
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320
Q

Bronchiolitis?

A

Acute bronchiolar inflammation. Most common cause of serious lower resp tract infection in <1yr olds (90% are 3-6m).

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321
Q

Pathogen that causes bronchiolitis in 75-80% of cases?

A

Respiratory syncytial virus (RSV)

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322
Q

What provides protection to newborns against RSV (causing bronchiolitis)?

A

maternal IgG

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323
Q

Higher incidence of bronchiolitis when?

A

winter

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324
Q

Causes of bronchiolitis?

A
  • RSV (most)
  • mycoplasa, adenoviruses
  • may be secondary bacterial infection
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325
Q

What can cause bronchiolitis to be more severe?

A

if bronchopulmonary dysplasia (eg. premature), congenital heart disease or CF

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326
Q

Features of bronchiolitis?

A
  • coryzal symptoms (eg. mild fever) precede:
  • dry cough
  • increasing SOB
  • wheezing, fine inspiratory crackles (not always)
  • feeding difficulties
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327
Q

Most often reason for hospital admission due to bronchiolitis?

A

feeding difficulties associated with increased dyspnoea

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328
Q

Immediate hospital admission (999 ambulance) in pts with bronchiolitis when?

A

any of…

  • apnoea
  • looks seriously unwell
  • severe resp distress= GRUNTING, marked chest recession, resp rate >70
  • central cyanosis
  • peristent O2 sats <92% on air
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329
Q

Consider hospital admission in pt with bronchiolitis when?

A

any of…

  • resp rate >60
  • difficulty feeding or inadequate oral fluid intake (50-75% of usual volume)
  • clinical dehydration
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330
Q

Ix for bronchiolitis?

A

immunofluorescence of nasopharyngeal secretions may show RSV

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331
Q

Mx for bronchiolitis?

A

Whilst awaiting hospital admission= supp O2 to all pts with O2 sats <92%

  • Largely supportive
  • humidified O2 via head box if O2 sats persistently <92%
  • NG feeding if can’t take enough fluid/feed my mouth
  • suction sometimes used for XS upper airway secretions
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332
Q

How to determine the severity of a child’s condition with bronchiolitis?

A
  • degree of agitation and consciousness (can be sign of hypoxia)
  • signs of exhaustion, cyanosis and invl. of accessory muscles of respiration at rest
  • examine chest, RR, pulse and BP
  • O2 sats on air (pulse oximetry)
  • hydration status= cap refill time, skin tugor and dryness of mucous membranes, urine output
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333
Q

Impending resp failure in pt with bronchiolitis may be indicated by what?

A

listlessness or decreased resp effort, recurrent apnoea, and/or failure to maintain O2 sats despite O2 supp

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334
Q

Low threshold for hospital admission in pt with bronchiolitis?

A
  • <3m
  • chronic lung disease
  • haemodynamically signif congenital heart disease
  • immunodef
  • born premature (esp. <32w)
  • long distance to healthcare in case of deterioration
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335
Q

What type of illness is bronchiolitis and when do symptoms tend to peak?

A

self-limiting
peak between 3-5d of onset

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336
Q

Mx advice is pt with bronchiolitis does not need hospital admission?

A
  • paracetamol/ibuprofen for fever and then for as long as child appears distressed
  • do not undress to try and reduce fever
  • regular fluids
  • check child regularly, incl. through the night
  • seek medical advice is child deteriorates
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337
Q

Sign of deterioration in child with broncholitis?

A
  • RR increaases
  • episodes of apnoea, cyanosis, increased effort of breathing (grunting, nasal flaring, marked chest recession)
  • fluid intake reduced to 50-75% of normal or signs of dehyration eg. dry mouth or no wet nappy for 12hrs
  • less responsive
  • worsening of fever
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338
Q

COPD stands for what?

A

chronic obstructive pulmonary disease

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339
Q

COPD?

A

Common treatable (but not curable) and largely preventable lung condition.
Persistent resp symptoms and airflow obstruction which is usually progressive and not fully reversible.

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340
Q

Major RF for development of COPD?

A

tobacco smoking

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341
Q

Cx of COPD?

A

reduced QOL and increased morbidity & mortality

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342
Q

Diagnosis/Ix for COPD?

A
  • Clinical +
  • Spirometry with BDR +
  • CXR (exclude other causes) +
  • FBC (identify anaemia or polycythaemia)
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343
Q

Spirometry findings in COPD?

A

A post bronchodilator FEV1/FVC of <0.7 (70%) confirms persistent airflow obstruction.

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344
Q

Mx for COPD?

A
  • info
  • smoking cessation
  • pnumococcal and influenza vaccine
  • pulmonary rehab
  • self-management plan
  • medical therapy
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345
Q

What is the use of ICSs in COPD associated with?

A

increased risk of pneumonia

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346
Q

When to refer to resp specialist in COPD?

A
  • lung ca, cor pulmonale or bronchiectasis suspected
  • very severe/worsening
  • <40yrs and/or FHx of A1AT def
  • uncertain
  • O2 therapy, long-term non-invasive ventilation therapy, long-tern oral corticosteroids or lung surgery being considered
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347
Q

Referral for pulmonary rehab in COPD is indicated when?

A
  • is functionally disabled by COPD
  • has had recent hospitalisation for acute exacerbation
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348
Q

Emergency admission for pt with acute exacerbation of COPD if?

A
  • severe SOB
  • inability to cope at home/living alone
  • poor or deteriorating condition
  • acute confusion/impaired consciousness
  • cyanosis or reduced O2 sats
  • worsening peripheral oedema
  • new arrhythmia
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349
Q

Mx of acute exacerbation of COPD not requiring admission?

A
  • increased dose of SABA
  • consider oral corticosteroids and an Abx
  • seek medical help if worsen rapidly or signif
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350
Q

All pts with COPD should be what?

A
  • followed up, frequency depending on their severity
  • end-of-life issues should be discussed and advance care planning offered when appropriate
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351
Q

Signs and symptoms of COPD?

A
  • SOB (persistent, progressive over time, worse on exertion)
  • chronic/recurrent cough
  • regular sputum production
  • frequent LRTI
  • wheeze
  • waking up at night with SOB
  • reduced exercise tolerance
  • cyanosis
  • raised JVP, peripheral oedema (may indicate cor pulmonale)
  • cachexia
  • hyperinflation of the chest
  • use of accessory muscles and/or pursed lip breathing
  • wheeze and/or crackles on auscultation
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352
Q

COPD auscultation?

A

wheeze and/or crackles

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353
Q

What may indicate cor pulmonale in COPD?

A
  • ankle swelling (peripheral oedema)
  • raised JVP
  • systolic parasternal heave
  • loud pulmonary second heart sound (over 2nd L ICS)
  • hepatomegaly
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354
Q

What symptoms are uncommon in COPD?

A

chest pain and haemoptysis uncommon- consider other causes

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355
Q

Cor pulmonale?

A

RHF secondary to lung disease. Caused by pulmonary HTN as a consequence of hypoxia.

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356
Q

Stages of severity of airflow obstruction (COPD) according to reduction in FEV1?

A

Post-BD FEV1/FVC= <0.7 (70%)

AND

Stage 1= mild- FEV1 80% of predicted or higher
2= moderate- 50-79%
3= severe- 30-49%
4= very severe- <30% or <50% with resp failure

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357
Q

Medical Research Council (MRC) dyspnoea scale?

A

Grade 1= not troubled by SOB except during strenuous exercise

2= SOB when hurrying or walking up slight hill

3= walks slower than others on the level because of SOB or has to stop for breath when walking at own pace

4= stops for breath after walking about 100m or after few mins on the level

5= too SOB to leave the house, or breathless when dressing/undressing

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358
Q

Differential diagnosis for COPD?

A
  • Asthma (nocturnal/variable symptoms, Hx atopic disease, non-smoker, <35yrs)
  • Bronchiectasis (copious sputum, freq chest infect, Hx of childhood pneumonia, coarse lung crepitations)
  • HF (SOB when lying flat, Hx of IHD, fine lung crepitations)
  • Lung ca (persistent cough, haemoptysis, weight loss or persistent hoarse voice)
  • Interstitial lung disease (dry cough, fine lung crepitations)
  • Anaemia (fatigue, SOB, palpitations)
  • TB (persistent productive cough, SOB, haemoptysis)
  • CF
  • Upper airway obstruction eg. tracheal tumour
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359
Q

Coarse crackles (crepitations)?

A
  • louder, low pitch, long lasting
  • like bubbling or crackling
  • during inspiration and expiration
  • typically in conditions where secretions or fluid present in larger airways:
  • pnuemonia
  • chronic bronchitis
  • late-stage pulmonary oedema
  • bronchiectasis
  • COPD exacerbation
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360
Q

Fine crackles (crepitations)?

A
  • soft, high pitched, brief
  • like velcro being pulled apart or hair rubbing near the ear)
  • mostly during inspiration
  • often in conditions affecting alveoli or small airways:
  • pulmonary fibrosis (common)
  • interstitial lung disease
  • early HF (pulmonary oedema)
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361
Q

Lung sounds associated with COPD?

A
  • wheezing (due to airway narrowing)
  • rhonchi (low pitch related to mucus in larger airways
  • diminished breath sounds in later stages (air trapping and hyperinflation)
  • coarse crackles during exacerbation
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362
Q

Crackles (crep) in pulmonary oedema?

A

fine crackles that may progress to coarse as fluid accumulates
- often associated with HF

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363
Q

Crackles (crep) in pulmonary fibrosis?

A

fine, late inspiratory crackles
“velcro crackles”

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364
Q

Crackles (crep) in bronchiectasis?

A

coarse crackles due to mucus build up in dilated airways

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365
Q

Crackles (crep) in pneumonia?

A

coarse crackles usually localised to area of lung infection

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366
Q

Early inspiratory crackles?

A

heard early during inspiration

often associated with chronic bronchitis or emphysema

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367
Q

Late inspiratory crackles?

A

heard later in inspiration

common in pulmonary fibrosis, HF and atelectasis

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368
Q

Examples of interstitial lung diseases?

A

asbestosis, pneumoconiosis, fibrosing alveolitis, sarcoidosis

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369
Q

Acute exacerbation of COPD definition?

A

sustained worsening of a pts symptoms from their usual stable state (beyond normal day to day variations)

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370
Q

Triggers of acute exacerbation of COPD?

A
  • resp tract infections eg. rhinovirus, h.influenzae, s.pneumoniae, moraxella catarrhalis
  • smoking
  • envrionmental pollutants
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371
Q

Common trigger of COPD exacerbation?

A

H.influenzae (most common)

rhinovirus

many exacerbations won’t respond to Abx as not caused by bacterial infections

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372
Q

CP of COPD exacerbation?

A

increased…
- SOB
- cough
- sputum production & change in sputum colour
- wheeze and chest tightness
- URTI symptoms eg. cold, sore throat
- reduced exercise tolerange
- ankle swelling
- increased fatigue
- acute confusion

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373
Q

Differential diagnosis of COPD exacerbation?

A
  • pneumonia
  • PE
  • pneumothorax
  • acute HF
  • cardiac ischaemia or arrhythmia
  • lung ca
  • upper airway obstruction
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374
Q

You should you not refer for pulmonary rehab if they have COPD?

A
  • unable to walk
  • unstable angina/recent MI
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375
Q

Oxygen is the treatment for what?

A

hypoxaemia not SOB

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376
Q

Inappropriate O2 therapy in pts with COPD may cause what?

A

resp depression

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377
Q

When to offer LTOT (long term O2 therapy) to pt with COPD?

A

Only after specialist assessment. Can improve survival in stable COPD and chronic hypoxia.

Refer for LTOT if…
- O2 sats 92% or less
- very severe or severe airflow obstruction
- cyanosis
- polycythaemia
- peripheral oedema
- raised JVP

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378
Q

Prophylactic Abx for COPD (initiated in secondary care)?

A

if have had 3+ exacerbating needing steroid therapy and at least 1 requiring hospital admission in previous yr= consider referral for Abx prophy

Azithromycin 500mg 3x per week for min 6-12m; assess benefit after 6m and 12m

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379
Q

Adverse effects of macrolides?

A

GI upset, hearing and balance disturbance, cardiac effects (prolongation of QTi) and microbio resistance

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380
Q

Follow up for COPD?

A

At least once per yr.
Very severe airway obstruction= twice per yr.

  • MRC D scale to assess severity
  • exacerbation freq and severity
  • meds incl. inhaler technqiue
  • smoking status and BMI
  • annual flu vaccine and once-only pneumococcal
  • Cx or cormorbities
  • Spiraometry
  • very severe= + pulse oximetry
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381
Q

What indicates rapidly progressing disease in COPD?

A

loss of 500ml or more over 5yr on spirometry

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382
Q

Target O2 sats for pt with COPD?

A

88-92% as risk of hypercapnia; adjust to 94-98% if pCO2 normal

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383
Q

SAMA?

A

short-acting muscarinic antagonist

eg. Ipratropium

slow onset: 30-60min and lasts 3-6hrs

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384
Q

LAMA?

A

long-acting muscarinic antagonists

eg. tiotropium

have prolonged binding to muscarinic receptors which lengthens duration of bronchodilator effect

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385
Q

SAMA for COPD?

A

ipratropium aerosol inhalation 1-2puffs (20-40ug) 3-4x daily

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386
Q

LAMA for COPD?

A

tiotropium (for maintenance)

Spiriva Respimat® 5 micrograms once daily by inhalation of aerosol (2 puffs is equivalent to 5 micrograms of tiotropium)

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387
Q

Causes of COPD?

A
  • smoking!
  • A1AT def
  • cadmium (used in smelting)
  • coal
  • cotton
  • cement
  • grain
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388
Q

Why is the use of peak flow limited in COPD?

A

can underestimate the degree of airflow obstruction

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389
Q

Offer LTOT to who in COPD?

A

pO2 of <7.3kPa or those with pO2 of 7.2-8kpa and one of:
- secondary polycythaemia
- peripheral oedema
- pulmonary HTN

assessment done by ABG on 2 occasions at least 3w apart in pts with COPD stable

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390
Q

When to not offer LTOT to pt with COPD?

A

if continue to smoke despite being offered smoking cessation advice

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391
Q

Risk assessment for LTOT?

A
  • smoking status
  • risks of falls from tripping over equipment
  • risk of burns and fires and increased risk of those who live in homes where someone smokes (incl. e-cigs)
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392
Q

Pts on LTOT for COPD should breathe the supp O2 for how long?

A

at least 15hrs a day

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393
Q

Things to do before starting azithromycin prophylaxis in pts with COPD who are indicated to have it?

A
  • LFTS and ECG to exclude QT prolongation
  • CT thorax to exclude bronchiectasis
  • Sputum culture to exclude atypical infections and TB
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394
Q

What can reduce risk of COPD exacerbations in pts with severe COPD and Hx of freq exacerbations?

A

Phosophodiesterase-4 (PDE-4) inhibitors eg. roflumilast

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395
Q

If pt has COPD and is said to have ‘asthma features’ (which affects COPD mx) what are these?

A
  • diagnosis of asthma or atopy
  • raised esosinophil count
  • substantial variation in FEV1 over time (at least 400ml)
  • substantial dinural variation in PEFlow (at least 20%)
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396
Q

Cystic fibrosis?

A

autosomal recessive disorder causing increased viscosity of secretions (eg. lungs and pancreas).

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397
Q

What causes CF?

A

defect in the cystic fibrosis transmembrane conductance regulator gene (CFTR) which codes a cAMP-regulated chloride channel

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398
Q

What does CFTR gene code for?

A

a cAMP-regulated chloride channel

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399
Q

Most cases of CF are due to what?

A

delta F508 on long arm of chromosome 7 causing defect in CFTR gene

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400
Q

CF affects how many births?

A

1 per 2500

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401
Q

Carrier rate or CF?

A

1 in 25

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402
Q

Organisms which may colonise CF pts?

A
  • Staph. aureus
  • P. aeruginosa
  • Aspergillus
  • Burkholderia cepacia (p. cepacia)
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403
Q

Diagnosis of CF?

A
  • +ve test result on infant screening (blood spot immunoreactive trypsin test) followed by sweat and gene tests to confirm

or

  • CP + sweat test (children & young adults) or gene test (adults)
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404
Q

Assess for CF (sweat test or gene test) in people with what?

A
  • FHx
  • congenital intestinal atresia
  • meconium ileus
  • distal intestinal obstruction syndrome
  • faltering growth
  • undernutrition
  • recurrent and chronic pulmonary disease
  • chronic sinus disease
  • obstructive azzoospermia
  • acute/chronic pancreatitis
  • malabsorption
  • rectal prolapse in children
  • pseudo-Barreter syndrome
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405
Q

Sweat test for CF?

A
  • abnormally high sweat chloride if have CF

CF= >60mEq/l
normal= <40mEq/l

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406
Q

Causes of false positive sweat test (when testing for CF)?

A
  • malnutrition
  • adrenal insufficiency
  • glycogen storage diseases
  • nephrogenic diabetes insipidus
  • hypothyroidism, hypoparathyroidism
  • G6PD
  • ectodermal dysplasia
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407
Q

Common reasons for false negative sweat test (when testing for CF)?

A

skin oedema, often due to hypoalbuminaemia/hypoproteinaemia secondary to pancreatic exocrine insuff

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408
Q

Features of CF?

A
  • neonatal (20%)= meconium ileus, less common: prolonged jaundice
  • recurrent chest infections (40%)
  • malabsorption (30%)= steatorrhoea, failure to thrive
  • other features (10%)= liver disease
  • short stature
  • DM
  • delayed puberty
  • rectal prolapse (due to bulky stools)
  • nasal polyps
  • male infertitlity, female subfertility
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409
Q

When are pts diagnosed with CF?

A

most on newborn screening or early childhood; 5% >18yrs

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410
Q

Meconium ileus in neonatal period can be sign of what?

A

CF

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411
Q

Recurrent chest infections, steatorrhoea, short stature, delayed puberty and male infertility?

A

CF

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412
Q

Symptoms/signs of malabsoption?

A

steatorrhoea, failure to thrive

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413
Q

Mx for CF? (7)

A

MDT approach

1) regular (2+ per d) chest physio and postural drainage (pts taught to do this); also deep breathing exercises
2) high calorie, high fat diet
3) minimal contact with other CF pts
4) vitamin supplements
5) pancreatic enzyme supplements taken with meals (Creon)
6) lung transplant

7) Lumacaftor/Ivacaftor (Orkambi)

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414
Q

Why should CF pts try to minimise contact with eachother?

A

to prevent cross infection with Burkholderia cepacia complex and Pseudomonas aeruginosa

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415
Q

What is an important CF specific contraindication to lung transplantation?

A

chronic infection with Burkholderia cepacia

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416
Q

Lumacaftor/Ivacaftor (Orkambi) for CF Mx?

A

used for CF pts who are homozygous for the delta F508 mutation

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417
Q

How does lumacaftor help pts with CF?

A

increased number of CFTR proteins that are transported to cell surface

418
Q

How does ivacftor help pts with CF?

A

a potentiator of CFTR that is already at the cell surface, increasing the probability that the defective channel will be open and allow chloride ions to pass through the channel pore

419
Q

Type of diet recommended for pts with CF?

A

high calorie and high fat

420
Q

Why do pts with CF get thick secretions?

A

Due to defect in CFTR gene that encodes for a protien (cAMP-regulated chloride channel) that functions as a chloride channel, which helps regulate movement of chloride and sodium across epithelial cells that line organs eg. lungs, pancreas and intestines.

  • Movement of chloride secretion is reduced and there is increased sodium absorption causing less water to be drawn into the mucus
  • Thicker sticky mucus in lungs= harder to clear and trap bacteria so chronic infections and inflam
  • Pancreas= thick secretions can block pancreatic ducts, preventing digestive enzymes reaching bowel so impairs digestion and absorption
  • Sinuses and reproductive system= mucus can causes blockages and Cx eg. sinus infections or infertility
421
Q

Drugs causing lung fibrosis?

A
  • amiodarone
  • cytotoxic agents: busulphan, bleomycin
  • anti-rheumatoid drugs: methotrexate, sulfasalazine
    nitrofurantoin
  • ergot-derived dopamine receptor agonists (bromocriptine, cabergoline, pergolide)
422
Q

Idiopathic pulmonary fibrosis (IPF) (previously called crytpogenic fibrosing alveolitis)?

A

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

423
Q

Causes of lung fibrosis?

A

medications, asbestos, connective tissue disease

424
Q

Cause of IPF?

A

no underlying cause

425
Q

IPF is typically seen in who?

A

men (2x as common); 50-70yrs

426
Q

Features of IPF?

A
  • progressive exertional dyspnoea
  • bibasal fine end-inspiratory crackles on auscultation
  • dry cough
  • clubbing
427
Q

Crackles in IPF?

A

bibasal fine end-inspiratory crackles on auscultation

428
Q

progressive exertional dyspnoea, bibasal fine end-inspiratory crackles on auscultation, dry cough, clubbing

A

IPF

429
Q

Diagnosis of IPF?

A
  • Spirometry
  • Impaired gas exchange- reduced transfer factor (TLCO)
  • Findings may be seen on CXR but high-resolution CT is GOLD for diagnosis
  • ANA +ve (30%); RF +ve (10%)
430
Q

Spirometry results for IPF?

A

restrictive picture (FEV1 normal/decreased, FVC decreased, FEV1/FVC increased)

431
Q

What may be seen on CXR for IPF (CT is gold for diagnosis)?

A

bilateral interstitial shadowing
(typically small, irregular, peripheral opacities - ‘ground-glass’ - later progressing to ‘honeycombing’)

432
Q

Mx for IPF?

A
  • pulmonary rehab
  • very few meds useful but pirfenidone (antifibrotic agent) may help in selected pts
  • many will need supp O2 and lung transplant eventually
433
Q

Prognosis of IPF?

A

poor
average life expectancy 3-4yrs

434
Q

bilateral interstitial shadowing (typically small, irregular, peripheral opacities - ‘ground-glass’ - later progressing to ‘honeycombing’) on CXR?

A

IPF

435
Q

Lung fibrosis in upper zones vs lower?

A

difficult to differentiate

most common causes (IPF and drugs) tend to affect lower zones

436
Q

Causes of lung fibrosis predominantly affecting the upper zones?

A

CHARTS

C - Coal worker’s pneumoconiosis
H - Histiocytosis/ hypersensitivity pneumonitis
A - Ankylosing spondylitis
R - Radiation
T - Tuberculosis
S - Silicosis/sarcoidosis

437
Q

Causes of lung fibrosis predominantly affecting the lower zones?

A
  • IPF
  • most connective tissue disorders (except ankylosing spondylitis) e.g. SLE
  • drug-induced: amiodarone, bleomycin, methotrexate
  • asbestosis
438
Q

Honeycombing on CXR/CT?

A

pulmonary fibrosis

439
Q

When might you suspect occupational asthma?

A
  • pts concerened that chemicals at work are worsening their asthma
  • Hx that symptoms are better at weekends/away from work
440
Q

Exposure to what chemicals is associated with occupational asthma?

A
  • isocyanates - most common cause; eg. spray painting and foam moulding using adhesives
  • platinum salts
  • soldering flux resin
  • glutaraldehyde
  • flour
  • epoxy resins
  • proteolytic enzymes
441
Q

What is recommended for pts with suspected occupational asthma?

A

serial measurements of peak expiratory flow at work and away from work

442
Q

Mx for suspected occupational asthma?

A

referral to resp

443
Q

Coal worker’s pneumoconiosis (or black lung disease)?

A

occupational lung disease caused by long term exposure to coal dust particles

444
Q

Pneumoconiosis?

A

accumulation of dust in the lungs and the response of the bodily tissue to its presence, most commonly used in relation to coal worker’s pneumoconiosis.

445
Q

Who most commonly experiences coal worker’s pneumoconiosis?

A

those who have been invl in coal mining industry or in populations with higher levels of exposure (areas with large coal mining industries); severity linked to extent of exposure; long lead time between first exposure and development of disease (around 15-20yrs after initial exposure).

446
Q

Pathophysiology of coal workers’ pneumoconiosis?

A

coal dust (2-5um in size) is inhaled and enters lungs -> reaches terminal bronchioles and engulfed by alveolar and interstitial macrophages -> dust particles then moved by macrophages via mucociliary elevator and removed from the body as mucus

In coal miners who are exposed over many yrs, the system is overwhelmed and the macrophages begin to accumulate in alveoli, starts an immune response causing damage to lung tissue

447
Q

Exposure to coal dust can lead to what presentations?

A

1) simple pneumonconiosis (most common; asymtomatic, increases risk of lung disease eg. COPD; may lead to PMF)

or

2) Progressive Massive Fibrosis (PMF)- 30% of those with stage 3 grading

448
Q

Staging of coal workers’ pneumoconiosis: simple pneumoconiosis?

A

graded by appearance on CXR

Category 1= some opacities but normal lung markings visible

Cat 2= large no. of opacities but normal lung markings visible

Cat 3= large no. of opacities with normal lung not visible

449
Q

Coal worker’s pneumoconiosis: Progressive Massive Fibrosis/complicated CWP?

A
  • duct exposure causes pt to develop round fibrotic masses which can be several cm in diameter
  • most common in upper lobes
  • often symptomatic= COB on exertion and cough, BLACK sputum (may have)
  • lung function testing= mixed obstructive/restrictive picture
450
Q

Ix for coal workers’ pneumoconiosis?

A
  • CXR= upper zone fibrosis
  • Spirometry= restrictive lung function tests: a normal or slightly reduced FEV1 and a reduced FVC
451
Q

Mx of coal workers’ pneumoconiosis?

A
  • avoid exposure to coal dust and other resp irritants eg. smoking
  • Mx symptoms of chronic bronchitis
  • Pts may be eligible for compensation via Industrial Injuries Act
452
Q

Silicosis?

A

fibrosing lung disease caused by inhalation of fine particles of crystalline silicon dioxide (silica)

453
Q

Silicosis is a risk factor for developing what?

A

TB (silica is toxic to marcophages)

454
Q

Occupations at risk of silicosis?

A
  • mining
  • slate works
  • foundries
  • potteries
455
Q

Features of silicosis?

A

upper zone fibrosing lung disease
‘egg-shell’ calcification of the hilar lymph nodes

456
Q

‘egg-shell’ calcification of the hilar lymph nodes

A

silicosis

457
Q

Legionnaire’s disease is caused by what?

A

intracellular bacterium Legionella pneumophilia

(legionella pneumonia)

458
Q

Where does Legionella pneumophilia colonise?

A

water tanks so may get from aircon or forgein holidays

459
Q

Transmission of Legionella pneumonia?

A

air-con or foreign holidays as it colonises in water tanks

person-person transmission NOT seen

460
Q

Features of Legionella pneumonia?

A
  • flue-like symptoms icl. fever
  • dry cough
  • relative brady
  • confusion
  • lymphopaenia
  • hyponataemia
  • deranged LFTs
  • pleural effusion (in 30%)
461
Q

Ix for Legionella?

A
  • Diagnostic= urinary antigen
  • CXR non-specific= mid-to-lower predominance of patchy consolidation; pleural effusion in 30%
462
Q

non-specific CXR signs incl. mid-to-lower zone predominance of patchy consolidation

A

Legionella pneumonia

463
Q

Mx of Legionella pneumonia?

A

erythromycin/clarithromycin

464
Q

Legionella pneumonia vs Mycoplasma pneumonia?

A

L= lymphopenia, hyponatraemia, diagnosis: urinary antigen

M= haemolytic anaemia/ITP, erythema multiforme, encephalitis/GBS, per/myocarditis, diagnosis: serology

Both= atypical pneumonia; flu like symptoms; dry cough; deranged LFTs; treat with macrolide eg. erythromycin

465
Q

Mycoplasma penumoniae is a cause of what?

A

atypical pneumonia often affecting younger pts

466
Q

Main Cx associated with mycoplasma pneumoniae?

A

erythema multiforme and autoimmune haemolytic anaemia

467
Q

Epidemics of Mycoplasma pneumoniae classically occur how often?

A

every 4yrs

468
Q

Why is it important to recognise atypical pneumonia?

A

may not respond to penicillins or cephalosporins due to it lacking a peptidoglycan cell wall

469
Q

Examples of atypical pneumonia?

A
  • mycoplasma
  • legionella
470
Q

Features of mycoplasma pneumoniae?

A
  • prolonged and gradual onset
  • flu-like symptoms precede a dry cough
  • bilateral consolidations on CXR
  • Cx may occur
471
Q

Cx associated with Mycoplasma pneumoniae?

A
  • cold agglutins (IgM): may cause an haemolytic anaemia, thrombocytopenia
  • erythema multiforme, erythema nodosum
  • meningoencephalitis, Guillain-Barre syndrome and other immune mediated neuro disease
  • bullous myringitis
  • pericarditis/myocarditis
  • GI: hepatitis, pancreatitis
  • renal: acute glomerulonephritis
472
Q

Bullous myringitis? (eg. Cx of Mycoplasma pneumoniae)

A

painful vesicles on tympanic membrane

473
Q

Ix for Mycoplasma pneumoniae?

A
  • Diagnosis= Mycoplasma serology
  • +ve cold agglutination test= peripheral blood smear may show RBC agglutination
474
Q

Mx of Mycoplasma pneumoniae?

A

doxycycline or a macrolide (eg. erythro/clarithromycin)

475
Q

Pneumonia?

A

infection of lung tissue in which the alveoli become filled with microorganisms, fluid, inflammatory cells which affect function of lungs

majority pts this is 2 to bacterial infection

476
Q

Most common type of pneumonia?

A

bacterial

viral and fungal less common

477
Q

Causes of pneumonia?

A
  • Strep. pneumoniae (pneumococcus)
  • H.influenzae
  • Staph.aureus
  • Mycoplasma pneumoniae
  • Legionella pneumonophilia
  • Klebsiella pneumoniae
  • Pneumocystis jiroveci
478
Q

Most common cause of pneumonia?

A

Strep.pneumoniae (pneumococcus) (80%)

  • high fever, rapid onset, herpes labialis (cold sores)
  • vaccine to pneumococcus is available
479
Q

Causes of CAP?

A
  • Strep.pneumoniae= most common
  • H.influenzae= pts with COPD
  • Moraxella= immunocompromised
480
Q

Causes of Atypical pneumonia?

A
  • Legionella= aircon eg. on holiday; rusty sputum
  • Chlamydiophilae psittacci= birds
  • Mycoplasma pneumoniae
  • Chlamydiophilae pneumoniae
481
Q

Causes of HAP?

A
  • psuedomonas aeruginose= most common
  • E.coli; Kelbsiella; s.aureus (MRSA)
482
Q

Staph.aureus pneumonia often occurs following what?

A

influenza infection

483
Q

Klebsiella pneumoniae classically seen in who?

A

alcoholics

484
Q

Pneumocystis jiroveci (fungal) is typically seen in who?

A

Pts with HIV

  • dry cough, exerise-induced desaturations and absence of chest signs
485
Q

Idiopathic interstitial pneumonia?

A

group of non-infective causes of pneumonia eg. cryptogenic organising pneumonia (form of bronchiolitis that may develop as a Cx of RA or amiodarone therapy)

486
Q

Majority of pts develop pneumonia where?

A

community-aquired pneumonia (CAP

487
Q

When is someone classed as having HAP?

A

pts who develop pneumonia within hospitals, occuring 48hrs or more after admission

488
Q

Signs and symptoms of pneumonia?

A

Symptoms= cough, sputum, dyspnoea, chest pain (may be pleuritic), fever

Signs= signs of systemic inflam response (fever, tachy); reduced O2 sats; auscultation= reduced breath sounds and bronchial breathing

489
Q

Classical CXR finding in pneumonia

A

consolidation

490
Q

Ix for pneumonia?

A
  • CXR= consolidation
  • FBC= neutrophilia if bacterial
  • U&Es= dehydration (U for urea in CURB65), other changes seen with some atypicals
  • CRP raised
  • sputum sample to diagnose causative organism
  • ABG if O2 low or pt has pre-existing resp disease eg. COPD
  • Legionella antibodies in intermediate or high risk pts
491
Q

Mx of pneumonia?

A
  • Abx
  • Supportive= O2 therapy if hypoxaemic; IV fluids if hypotensive or signs of dehydration
492
Q

Mx of pts with CAP is usually determined according to a risk score called what?

A

CURB-65 (CRB-65 if primary care as can’t get serum urea)

493
Q

CURB-65 score stands for what?

A

C= confusion (abbreviated metal test score <=8/10

U= urea/BUN >19mg/dL (>7mmol/L urea)

R= resp rate >=30

B= systolic BP <90mmHg or diastolic BP <=60

Age >=65

494
Q

CRB-65 score in primary care is used for what?

A

to decide whether pt with CAP requires hospital admission:

3+= urgent admission
1 or 2= consider
0= Mx at home considered

495
Q

Abx for CAP?

A

amoxicillin 500mg 3xd 5d

if atypical suspected or allergy= doxycycline 200mg 1st day then 100mg od 4d OR clarithromycin 500mg 2xd 5d OR erythromycin (pregnancy) 500mg 4xd 5d

496
Q

Expected speed of improvement of pnuemonia symptoms once started Abx?

A

1w= fever resolved
4w= chest pain & sputum production reduced
6w= cough and SOB reduced
3m= mostly resolved but fatigue may still be present
6m= fully resolve

497
Q

Arrange a CXR 6w after Mx for pneumonia in who?

A
  • S&S persist despite Mx
  • higher risk of malignancy eg. smokers and >50yrs
498
Q

Prognosis of pneumonia?

A

CURB-65 score also correlates with an increased risk of mortality at 30 days with patients with a CURB-65 score of 4 approaching a 30% mortality rate at 30 days.

499
Q

Mx of low-severity CAP?

A

amoxicillin 1st line 5d

allergic= macrolide or tetracycline

500
Q

Mx of moderate and severe CAP?

A

dual Abx therapy= amoxicillin + macrolide 7-10d

if high severity use co-amoxiclav +macrolide
( beta-lactamase stable penicillin)

501
Q

When to not discharge pt with pneumonia?

A

DO NOT if have 2+ of:

  • T >37.5
  • RR 24+
  • HR >100bpm
  • SBP 90 or less
  • O2 sats <90% on air
  • abnormal mental status
  • inability to eat without assistance
502
Q

Why is CRP measured in pts with pneumonia?

A

monitored in admitted pts to help determine response to Mx and also can be used to determine Abx is needed

CRP <20mg/L= do not routinely offer Abx
20-100= consider delayed prescription
>100= Abx

503
Q

What does consolidation look like on CXR?

A

opacity in the area of infection

504
Q

Pneumothorax definition?

A

accumulation of air in the pleural space, resulting in partial or complete collapse of affected lung

505
Q

Types of pneumothoraxes?

A
  • Spontaneous P
  • Traumatic P
  • Tension P
  • Iatrogenic P
  • Catamenial P
506
Q

Types of spontaneous pnuemothorax?

A
  • primary spontaneous P (PSP)
  • secondary spontanous P (SSP)
507
Q

Primary spontaneous pneumothorax?

A
  • no underlying disease
  • tall, thin, young individuals most commonly affected; smokers
  • Caused by/associated with rupture of subpleural blebs or bullae
508
Q

Secondary spontaneous pneumothorax?

A
  • in pre-existing lung disease eg. COPD, asthma, CF, lung ca, pneumocystis pneumonia
  • connective tissue diseases eg. Marfan’s also a RF
509
Q

Traumatic pneumothorax?

A

results from penetrating or blunt chest trauma, leading to lung injury and pleural air accumulation

510
Q

Tension pneumothorax?

A

severe, results in displacement of mediastinal structures that may result in severe resp distress and haemodynamic collapse

511
Q

Iatrogenic pneumothorax?

A

occurs as Cx of medical procedures eg. thoracentesis, central venous catheter placement, ventilation, non-invasive ventilation, lung biopsy

512
Q

Catamenial pneumothorax?

A

cause of 3-6% of spontaneous Ps occurring in menstruating women; thought to be caused by endometriosis within the thorax

513
Q

Symptoms and signs of pneumothorax?

A

Symptoms= sudden; dyspnoea, pleuritic chest pain

Signs= hyper-resonant lung percussion; reduced breath sounds; reduced lung expansion; tachypnoea; tachycardia

514
Q

3 signs of tension pneumothorax?

A
  • resp distress
  • tracheal deviation away from side of pneumothorax
  • hypotension and tachy if severe so shocked
515
Q

Resp distress, tracheal deviation away from area an d hypotension?

A

tension pneumothorax

516
Q

Mx of pneumothorax?

A

1) is pt symptomatic?
- No or minimal= conservative regardless of size
- Yes= next step

2) Are there high risk characteristics?

3) Is it safe to intervene?

4) Safe and no high risk= choice of conservative, ambulatory device or needle aspiration (depending on pt preference and local availability)

4) Safe but high risk= chest drain

517
Q

High risk characteristics of pneumothorax?

A
  • haemodynamic compromise (tension pneumothorax)
  • signif hypoxia
  • bilateral pneumothorax
  • underlying lung disease
  • > =50yrs with signif smoking Hx
  • haemothorax
518
Q

How is it determined if it is safe to intervene in pneumothorax Mx? (before needle aspiration or chest drain insertion)

A

usually:
2cm laterally or apically on CXR OR any size on CT scan which can be safely accessed with radiological support

519
Q

Conservative care for pneumothorax?

A
  • PSP managed conservatively should be reviewed every 2-4d as outpt
  • SSP managed conservatively should be monitored as inpatient
  • stable= follow up in outpts in 2-4w
520
Q

Ambulatory care for pneumothorax?

A
  • eg. Rocketµ Pleural Vent: FG catheter mounted on an 18G needle and a pigtail catheter to minimize the risk of occlusion
  • have one way valve and vent to prevent air and fluid return to pleural space while allowing for controlled escape of air and drainage of fluid
  • many also have indication diaphragm that signals the catheter tip enters the pleural space and continues to fluctuate with respiration, aiding assessment of P resolution
521
Q

Needle aspiration for pneumothorax?

A
  • chest drain inserted if needle aspiration unsuccessful
  • if resolved, discharge and follow up in outpt in 2-4w
522
Q

Chest drain review for pneumothorax?

A
  • daily review as inpt
  • remove drain when resolved
  • discharge and follow up in outpt in 2-4w
523
Q

Where is a chest drain inserted for pneumothorax?

A

in triangle of safety= 5th ICS, midaxillary line and anterior axillary line

just above rib to avoid neurovascular bundle

CXR after to check position

524
Q

Cx of chest drain?

A
  • air leaks around drain site= persistent bubbling of fluid
  • surgical emphysema= air collects in subcut tissue
525
Q

Ix for pneumothorax?

A

1st= Erect CXR: measure horizontally from lung edge to inside of the chest wall at the level of the hilum
1st= clinical

  • If P too small= CT thorax
526
Q

Mx for persistent or recurrent pneumothorax (persistent air leak or insuff lung reexpansion despite chest drain insertion, or recurrent P)?

A

Video-assisted thoracoscopic surgery (VATS) to allow for mechanical/chemical pleurodesis +/- bullectomy

527
Q

Discharge advise following pneumothorax?

A
  • avoid smoking
  • contraindication to fly= must wait to 1w post check CXR or after 2w after successful drainage and no residual air
  • Scuba diving should be permanently avoided unless pt has undergone bilateral surgical pleurectomy and has normal lung function and chest CT scan postop
528
Q

What does tension pneumothorax result in?

A

life-threatening; accumulation of air in pleural space under +ve pressure, leading to collapse of lung on affected side and shift of the mediastinum towards the contralateral side; results in impaired venous return to heart and so reduction in cardiac output posing signif risk of cardiovascular collapse

529
Q

Causes of tension pneumothorax?

A
  • trauma: penetrating or blunt chest trauma
  • iatrogenic: thoracentesis; central venous catheter placement; positive pressure mechanical ventilation
  • spontaneuous: particularly if underlying lung disease eg. COPD or CF; lung blebs (small blisters on lung surface) can rupture spontaneously causing air to leak into pleural space
530
Q

Pathophysiology of tension pneumothorax?

A

air enters pleural space and is unable to escape -> creates one way valve effect (due to flap of tissue acting as a valve or similar mechanism in traumatic/iatrogenic wound) -> continuous accumulation of air leads to increased intrapleural pressure which exceeds atmospheric pressure throughout the resp cycle -> as intrapleural pressure rises, it exerts several deleterious effects

531
Q

Effects of tension pneumothorax?

A
  • lung collapse
  • mediastinal shift
  • impaired venous return
  • reduced cardiac filling
532
Q

Tension pneumothorax: lung collapse?

A

affected lung compressed -> decrease in functional residual capacity and impaired gas exchange

533
Q

Tension pneumothorax: mediastinal shift?

A

increased pressure pushed mediastinum towards the contralateral side; shift can compress the opposite lung further impairing lung function.
Tracheal deviation (late sign) is key diagnostic indicator.

534
Q

Tension pneumothorax: impaired venous return?

A

Mediastinal shift and raised intrathoracic pressure compress the great veins reducing venous return to the heart. This diminishes cardiac output and can lead to obstructive shock: hypotension and tachycardia/

535
Q

Tension pneumothorax: reduced heart filling?

A

Direct pressure on the heart, coupled with reduced venous return, impairs both RV & LV filling; can lower cardiac output and SBP.

536
Q

Signs and symptoms of tension pneumothorax?

A
  • acute onset dyspnoea
  • pleuritic chest pain
  • tachypnoea
  • hyperresonance on percussion, diminished breath sounds on affecterd side
  • tracheal deviation away from affected side
  • severe= shock: hypotension and tachycardia
537
Q

Ix for tension pneumothorax?

A

CLINICAL, do not await imaging before Mx

538
Q

Aim of Mx of tension pneumothorax?

A

decompression of pleural space

539
Q

Mx of tension pneumothroax?

A

Needle thoracostomy= insert a large bore cannula into the 2nd ICS in midclavicular line on affected side
Then follow this by placement of chest drain (tube thoracostomy) in the safe triangle of chest to allow continuous drainage of air for definitive Mx

540
Q

Pulmonary arterial hypertension (PAH) defined as what?

A

resting mean pulmonary artery pressure of >=20mmHg

541
Q

What is thought to play a key role in pathogenesis of PAH?

A

endothelin

542
Q

Pulmonary arterial HTN is more common in who?

A

females
30-50yrs

543
Q

What increases risk of pulmonary arterial HTN?

A

HIV, cocaine, anorexigens (eg. fenfluramine), inherited (autosomal dominant)

544
Q

What may pulmonary arterial HTN develop secondary to what?

A

chronic lung diseases eg. COPD

545
Q

Features of pulmonary arterial HTN?

A
  • progressive exertional dyspnoea
  • exertional syncope
  • exertional chest pain
  • peripheral oedema
  • cyanosis
546
Q

What are the examination findings of pulmonary arterial HTN?

A

R ventricular heave, loud P2, raised JVP with prominent ‘a’ wave, tricuspid regurg

547
Q

Mx of pulmonary arterial HTN?

A
  • TUC eg. anticoag, oxygen

+ve response to acute vasodilator testing (minority)= oral CCB

-ve response (majority)= prostacyclin analogues (treprostinil, iloprost); endothelin receptor antagonists (non-selective: bosentan; selective a of endothelin receptor A: ambrisentan); phosphodiesterase inhibitors= sildenafil

Progressive symptoms= consider heart-lung transplant

548
Q

Ix to decide on Mx for pulmonary arterial HTN?

A

Acute vasodilator testing

549
Q

Acute vasodilator testing to decide on Mx for pulmonary arterial HTN?

A

aims to decide which pts show signif fall in pulmonary arterial pressure following the administration of vasodilators eg. IV epoprostenol or inhaled nitric oxide

550
Q

Pulmonary HTN defined as?

A

sustained elevation in mean pulmonary arterial pressure >20 at rest

551
Q

How many groups of pulmonary HTN?

A

5

552
Q

Pulmonary HTN: group 1?

A

PAH:
- idiopathic
- familial
- associated conditions: collagen vascular disease; congen heart disease with systemic to pulmonary shunts; HIV; drugs and toxins; sickle cell
- persistent pulmonary HTN of the newborn

553
Q

Pulmonary HTN: group 2?

A

Pulmonary HTN with left heart disease:
- leftsided A, V or valvular disease eg. LV systolic and diastolic dysfunction; mitral stenosis and mitral regurg

554
Q

Pulmonary HTN: group 3?

A

Pulmonary HTN secondary to lung disease/hypoxia:
- COPD
- interstitial lung disease
- sleep apnoea
- high altitude

555
Q

Pulmonary HTN: group 4?

A

Pulmonary HTN due to thromboembolic disease

556
Q

Pulmonary HTN: group 5?

A

Pulmonary HTN due to miscellaneous conditions:
- lymphangimatosis eg. secondary to carcinomatosis or sarcoidosis

557
Q

5 causes of pulmonary HTN?

A

1) Pulmonary arterial HTN (PAH)

2) PHTN with left heart disease

3) PHTN secondary to lung disease/hypoxia

4) PHTN due to thromboembolic disease

5) PHTN due to miscellaneous conditions

558
Q

Pulmonary embolism?

A

Life-threatening condition which one or more emboli, usually arising from a blood clot formed in the veins, are lodged in and obstruct the pulmonary arterial system, causing severe resp dysfunction

559
Q

Major source of a PE?

A

deep vein thrombosis (DVT) in lower limb

560
Q

RFs for PE?

A
  • DVT
  • recent surgery
  • signif immboility eg. wheelchair
  • previous DVT or PE
  • active ca
  • long-duration travel
  • COCP/HRT
  • antiphospholipid syndrome
  • lower limb trauma
  • recent MI
  • increasing age
  • FHx DVT
  • pregnancy, esp. 6w postpartum
  • ciagrette smoking
  • obesity
561
Q

Cx of PE?

A

chronic thromboembolic pulmonary hypertension

untreated= high risk of death

562
Q

Suspect PE in who? (CP)

A

1 or more of:
dyspnoea, haemoptysis, chest pain, syncope/pre-syncope, tachypnoea, features of DVT

563
Q

When to arrange immediate admission to hospital in pt with suspected PE?

A
  • has signs of haemodynamic instability
  • is pregnant or has given birth within 6w
564
Q

What should be used to estimate the clinical probability of PE (except if haemodynamically unstable, pregnant or given birth <6w)?

A

two-level PE Wells score

565
Q

2-level PE Wells score of >4

A

PE likely

566
Q

What does CTPA stand for?

A

computed tomography pulmonary angiogram

567
Q

2-level PE Wells score of 4 points or less?

A

PE unlikely

568
Q

What to do if pt has 2-level PE Wells score of >4 and so a PE is likely?

A
  • hospital admission for immediate CTPA
  • if can’t be done
    immediately then interim therapeutic anticoag + hospital admission
569
Q

What to do if pt has 2-level PE Wells score of 4 or less and so a PE is unlikely?

A
  • D-dimer test with results available within 4hrs
  • if >4hrs then interim therapeutic anticoag whilst waiting results
  • if D-dimer +ve= immediate CTPA (same as if PE likely on Wells)
  • D-dimer -ve= stop anticoag and consider alternative diagnosis
570
Q

Mx of confirmed PE?

A

anticoag in secondary care

571
Q

Follow up in primary care following PE?

A
  • monitor treatment
  • anticoag info book and anticoag alert card
572
Q

What to offer during follow up of an unprovoked PE?

A

Ix to assess possibility of undiagnosed cancer, hereditary thrombophilia testing or antiphospholipid antibodies.
Must stop anticoag before.

573
Q

Signs of PE?

A

may have…
- elevated JVP
- fever
- gallop rhythm, wide split-2nd HS, tricuspid regurg
- hypotension and cardiogenic shock (haemodyn instab rare and indicates central/extensive PE with severely reduced haemodyn reserve)
- hypoxia
-pleural rub
- tachycardia

574
Q

Symptoms of PE?

A
  • dyspnoea
  • haemoptysis
  • pleuritic or one sided chest pain
  • syncope/pre-syncope
  • tachypnoea
  • features of DVT

may have…
- retrosternal chest pain (due to RV ischaemia)
- cough

575
Q

ECG signs that may be present in pt with PE?

A

sinus tachycardia may be seen

large S wave in lead I, large Q in lead III and inverted T in lead III (S1Q3T3) but only in 20% pts

RBBB and right axis deviation also associated

576
Q

PE differential diagnosis?

A
  • acute bronchitis
  • exacerbation of asthma
  • exacerbation of COPD
  • pneumonia
  • pneumothorax
  • ACS
  • acute CHF
  • aortic dissection
  • cardiac tamponade
  • MI
  • pericarditis
  • unstable angina
  • MSK chest pain (can be present with PE)
  • GORD
  • panic disorder
  • causes for collapse= arrythmias, stroke/TIA, orthostatic hypotension, seizures, vasovagal syncope
  • non-thrombotic sources of emboli= air; amnitoic fluid; fat (pelvic/long bone fracture); forgein material; sepsis; tumours (prostate, GI, liver, kidney, breast)
577
Q

Signs of haemodynamic instability?

A
  • cardiac arrest
  • obstructive shock: SBP <90
  • persistent hypotension
578
Q

How is persistent hypotension defined?

A

SBP less than 90 mmHg or a drop in SBP of 40 mmHg or more, lasting longer than 15 minutes and not caused by new-onset arrhythmia, hypovolaemia, or sepsis.

579
Q

How is obstructive shock defined?

A

SBP of less than 90 mmHg or vasoactive drugs required to achieve a BP of 90 mmHg or more despite adequate filling status, plus end-organ hypoperfusion (altered mental status, cold, clammy skin, oliguria/anuria, increased serum lactate).

580
Q

2-level PE Wells score features?

A

Clinical features of deep vein thrombosis (DVT; minimum of leg swelling and pain with palpation of the deep veins) = 3

An alternative diagnosis is less likely than PE= 3

Heart rate greater than 100 beats per minute= 1.5

Immobilization for more than 3 days or surgery in the previous 4 weeks= 1.5

Previous DVT or PE= 1.5

Haemoptysis= 1

Cancer (receiving treatment, treated in the last 6 months, or palliative)= 1

581
Q

Interim therapeutic anticoag for PE if required?

A

apixaban or rivaroxaban

582
Q

What to do for people starting interim anticoag therapy?

A

Baseline bloods= FBC, renal and hepatic function, PT, APTT

don’t wait on results before starting Tx

583
Q

Secondary care Mx for PE?

A

1st= DOAC (apixaban or ribaroxaban)
- If not suitable= LMWH for 5d then dabigatran or edoxaban OR LMWH + VKA (vit K antagonist) 5d or until INR is 2+ in 2 consec readings, then VKA on own

Haemodynamically unstable= Thrombolytic therapy

Repeat embolisms despite anticoag=Inferior vena cava (IVC) filters

584
Q

Inferior vena cava (IVC) filters for PE?

A

trap fragmented thromboemboli from the deep leg veins en route to the pulmonary circulation (whilst preserving blood flow in the IVC filter)

if anticoagulation is contraindicated or PE has occurred during anticoagulation treatment.

585
Q

Thrombolytic therapy for PE?

A
  • thrombolytic agent can either be given into a peripheral vein (systemic thrombolysis) or directly into the pulmonary arteries via a catheter (catheter-directed thrombolysis).
  • Open pulmonary embolectomy (surgical removal of clots in the pulmonary arteries) is an alternative used less commonly in modern practice.
586
Q

Triad for PE (rare it actually fits this in real world)?

A

pleuritic chest pain, haemoptysis and dyspnoea

587
Q

What Ix for PE is prefered if there is renal impairment?

A

V/Q scan as doesn’t require contract like in CTPA

588
Q

Why is CTPA used and is better than V/Q scanning for PE?

A

speed, easier to perform out-of-hours, a reduced need for further imaging and the possibility of providing an alternative diagnosis if PE is excluded

589
Q

D-dimer for PE?

A
  • sensitivity = 95-98%, but poor specificity
  • age-adjusted D-dimer levels should be considered for patients > 50 years
590
Q

CXR in PE?

A

normal but can have wedged-shaped opacification

can used to exclude other pathology

591
Q

Causes of V/Q mismatch?

A

old PE, AV malformations, vasculitis, previous radiotherapy

592
Q

What may be missed in CTPA for PE?

A

peripheral emboli affecting subsegmental arteires

593
Q

Anticoag Tx for how long if have PE?

A

3m if provoked

3-6m if active ca

6m if unprovoked

594
Q

First line anticaog for PE?

A

DOACs= apixaban or ribaroxaban for 3m

  • If renal impairment severe (<15) then LMWH
  • If antiphospholipid syndrome= LMWH + VKA
595
Q

Assess bleeding risk?

A

ORBIT score

596
Q

Dose of apixaban for PE? Rivaroxaban?

A

A= 10mg 2xd for 7d then maintenance 5mg 2xd

R= 15mg 2xd 21d, to be taken with food, then maintenance 20mg od

597
Q

Key indications for non-invasive ventilation (NIV)?

A
  • COPD with resp acidosis pH 7.25-7.35
  • T2RF secondary to chest wall deformity, neuromuscular disease or obstructive sleep apnoea
  • cardiogenic pulmonary oedema unresponsive to CPAP
  • weaning from tracheal intubation
598
Q

Recommended initial settings for bi-level pressure support in COPD?

A
  • expiratory +ve airway pressure (EPAP)= 4-5cm H2O
  • inspiratory +ve airway pressure (IPAP)= 12-15cm H2O
  • back up rate= 15 breaths/min
  • back up inspiration:expiration ratio= 1:3
599
Q

What is respiratory failure?

A

inability of the resp system to maintain adequate gas exchange

600
Q

Type 1 resp failure?

A

↓ pO2 with a
normal or ↓ pCO2

601
Q

Type 2 resp failure?

A

↑ pCO2 with a normal or ↓ pO2

602
Q

What do you get in T1RF?

A

hypercapnia → ↓ pH → respiratory acidosis

603
Q

Causes of T1RF?

A
  • pneumonia
  • PE
  • asthma
  • pulmonary oedema
  • acute resp distress syndrome
604
Q

Causes of T2RF?

A
  • COPD
  • decompensation in other resp conditions eg. life threatening asthma/pulmonary oedema
  • neuromuscular disease
  • obesity hypoventilation syndrome
  • sedative drugs: benzos, opiate overdose
605
Q

What drugs can cause T1RF?

A

sedatives eg. benzodiazepines; opiate overdose

606
Q

Sarcoidosis?

A

Multisystem disease of unknown aetiology.
Characterised by the presence of non-caseating granulomas (non-necrotising nodules of inflammation and scarring)

607
Q

What condition is characterised by the presence of non-caseating granulomas (non-necrotising nodules of inflam and scarring)?

A

Sarcoidosis

608
Q

Most commonly affected organs affected in sarcoidosis?

A

1) lungs (90% pts)
2) skin (30%)
3) eyes (30%), brain, NS, liver, heart

609
Q

Cause of sarcoidosis?

A

Unknown; may be due to inflam response to environmental agent or infection in genetically predisposed individuals

610
Q

Prognosis/disease course of sarcoidosis?

A

2/3 remission within 2-5yrs with majority requiring no Tx.

25% develop residual fibrosis in lungs or elsewhere

10-30% pts: disease will become chronic and require prolonged Tx

611
Q

CP of sarcoidosis?

A
  • can be asymptomatic: detected incidental on CXR
  • dyspnoea
  • persistent cough
  • wheezing
  • non-cardiac chest pain
  • skin changes: hyper/hypopigmentation; keloid reaction; erythema nodosum
  • eye invl: uveitis
  • Fatigue and mood disturbance
  • peripheral lymphadenopathy: C submand nodes (non-tender)
  • Hepatic: megaly (non-tender), RUQ pain
  • Neuro: VII nerve palsy, headaches, seizures
  • MSK: acute arthritis of lower legs, ankles, knees, fingers
  • Renal: kidney stones (due to abnorm Ca metabolism)
612
Q

Ix for sarcoidosis?

A

1) CXR
2) Chest CT if CXR suggests sarcoidosis
3) Bloods:
LFTs (ALP elevated);
U&Es (hypercalcaemia); FBC (lymphopenia, leukopenia and/or anaemia)
4) ECG: ?cardiac invl and/or pulmonary HTN
5) Spirometry= may show restrictive

4) then refer to secondary care to confirm
eg. tissue biopsy= non-caseating granulomas

613
Q

Mx for sarcoidosis?

A

If Tx required:

1st= corticosteroids (topical/oral)- sufficient with only skin/eye invl only

2nd line= immunosupressants eg. methotrexate

3rd= biologics eg. anti-TNF drugs such as infliximab

614
Q

Monitoring for sarcoidosis?

A

1) stage 1 pulmonary S= monitoring for up to 2yrs to assess remission or progression

2) Stage II-IV P S= likely to need longer term monitoring

3) signif extrapulmonary invl= long term monitoring every 6m

4) withdrawing from corticosteroids= ongoing monitoring

615
Q

Skin invl. in sarcoidosis?

A

espec face, hands, legs

  • hyper/hypopigmentation
  • erythema nodosum
  • Lupus pernio
  • prutitus, purple-red or borwn thickened circular plaques and sarcoidosis of scars and tattoos
616
Q

Lupus pernio?

A

specific to sarcoidosis and is suggested by large bluish-red and dusky purple infiltrated nodules and plaque-like lesions on the nose, cheeks, ears, fingers and toes

617
Q

What would CXR in sarcoidosis show?

A
  • isolated bilateral hilar lymphadenopathy
  • diffuse infiltrates and disseminated nodules
  • fibrosis in upper lobes
618
Q

What would chest CT show in sarcoidosis?

A

granulomatous inflam along lymphatic tracts

619
Q

Bloods in sarcoidosis?

A
  • LFTs= elevated ALP
  • U&Es= hypercalcaemia
  • FBC= lymphopenia, modest leukopenia and/or anaemia
  • Renal= urea and serum creatinine elevated if renal involvement
620
Q

Elevated ALP, lymphopenia and hypercalcaemia on bloods + isolated bilateral hilar lymphadenopathy on CXR + granulomatous inflam along lymphatic tracts?

A

sarcoidosis

621
Q

Staging of sarcoidosis?

A

CXR findings:

0= normal

I= enlarged nodes only (BHL)

II= enlarged nodes + parenchymal changes (BHL + intersitial infiltrates)

III= parenchymal changes without enlarged nodes or fibrosis (diffuse intersitial infiltrates only)

IV= fibrosis

622
Q

Who to refer pt with sarcoidosis to if more than one affected organ system?

A

MDT

623
Q

Ix in secondary care for sarcoidosis to confirm diagnosis, determine severity and identify extra-pulmonary invl.?

A

bronchoscopy; tissue biopsy; CT; PET and MRI can be useful.
echo if ?cardiac invl.

624
Q

When in Mx for sarcoidosis indicated?

A

dangerous disease and/or unacceptable loss of QOL

eg. stage 2/3 symptomatic; hypercalcaemia or eye, heart or neuro invl.

625
Q

When may palliative care arrangements be needed for pt with sarcoidosis?

A

progressive fibrotic pulmonary sarcoidosis with resp failure

626
Q

Differential diagnosis for sarcoidosis?

A
  • TB
  • non-small-cell lung ca
  • lymphoma
  • CHF
  • idiopathic pulmonary fibrosis
  • drug induced fibrosis
  • pulmonary fibrosis caused by connective tissue diseases
  • Berylliosis (Hx of employment in nuclear and aerospace industries)
  • Silicosis (Hx in mining, quarrying or stonemasonry)
  • Hypersensitivity pneumonitis
  • Histoplasmosis (Hx of living in endemic area eg. South America, continental Africa, Madagascar)
627
Q

Who is sarcoidosis more common in?

A

young adults & people of African descent

628
Q

Acute and insidious features of sarcoidosis?

A

Acute= erythema nodosum; bilateral hilar lymphadenopathy; swinging fever; polyarthralgia

Insidious= dyspnoea, non-productive cough, malaise, weight loss

629
Q

Why can you get hypercalcaemia in sarcoidosis?

A

macrophages inside granulomas cause increased conversion of Vit D to its active form (1,25-dihydroxycholecalciferol)

630
Q

Syndromes associated with sarcoidosis?

A
  • Lofgren’s syndrome
  • Heerfordt’s syndrome (uveoparotid fever)
  • Mikulicz syndrome (unhelpful as overlap with Sjogren’s)
631
Q

Lofgren’s syndrome?

A

acute form of sarcoidosis characterised by bilateral hilar lymphadenopathy (BHL), erythema nodosum, fever and polyarthralgia.

excellent prognosis

632
Q

Heerfordt’s syndrome (uveoparotid fever)?

A

associated with sarcoidosis

parotid enlargement, fever and uveitis secondary to sarcoidosis

633
Q

Mikulicz syndrome?

A

outdated and unhelpful as overlap with Sjogren’s

enlargement of parotid and lacrimal glands due to sarcoidosis, TB or lymphoma

634
Q

What would tissue biopsy for sarcoidosis show?

A

non-caseating granulomas

635
Q

Factors in sarcoidosis associated with poor prognosis?

A
  • insidious onset, symptoms > 6 months
  • absence of erythema nodosum
  • extrapulmonary manifestations: e.g. lupus pernio, splenomegaly
  • CXR: stage III-IV features
  • black African or African-Caribbean ethnicity
636
Q

What is tuberculosis caused by?

A

bacteria- members of the Mycobacterium tuberculosis complex

637
Q

How is TB spread?

A

inhaling via resp droplets released when a person with pulmonary or laryngeal TB coughs

638
Q

2 types of TB

A

active disease and latent

639
Q

Active TB?

A

symptomatic or progressive disease of the lung (most common) and/or other organs (extrapulmonary TB)

640
Q

Latent TB?

A

no clinically active TB (asymptomatic and not infectious)

641
Q

RFs for TB?

A

born in high prevalence area, children, adult males, people with previously untreated infection, close contact with active TB, immunosuppressive conditions or drugs, under-served groups

642
Q

Suspect TB in who?

A

weight loss, fever, night sweats, anorexia, malaise, RFs for TB

pulmonary invl= persistent productive cough, haemoptysis, dyspnoea

extrapulmonary= organ-specific S&S

643
Q

Ix for TB

A

?active pulmonary= CXR + 3 spontaneously produced sputum samples

?active extrapul= same as above + Ix depending on likely site of disease

  • can do sputum smear= stained for acid-fast bacilli (Ziehl-Neelsen stain), but all mycobacteria will stain +ve (even nonTB)
644
Q

Asymptomatic people who are at risk of TB should be screened through the local multidisciplinary TB team, including who?

A
  • people in contact with pt with active pulmonary or laryngeal TB (contact tracing needed)
  • immunocompromised at high risk for latent TB
  • new entrants to UK from high TB prevalence country, who present to healthcare services and not had pre-entry screening
  • new NHS employees who will be working with pts or clinical specimens
  • evidence of TB scarring or untreated fibrotic changes on CXR
645
Q

What if pt has known active or latent TB but not completed treatment as planned?

A

re-referral to local multidisciplinary TB team

646
Q

Primary care Mx of pt with confirmed active TB?

A
  • encourage adherence to specialist Tx
  • smoking cessation & lifestyle
  • pulmonary or larygneal TB can be transmitted to close contacts and screening via contact tracing will be arranged by local specialist team
  • symptoms suggesting relapse after finishing Tx need to inform primary care/local specialist team immediately
647
Q

Why may active TB be difficult to detect so may be diagnositic delays or misdiagnosis?

A

onset can be insidious and early stages may be difficult to detect

648
Q

Is dyspnoea and haemptysis an early or late feature of TB?

A

late

649
Q

examples of possible extra-pulmonary invl. in TB?

A
  • Lymphadenopathy (painless, Cervical or supraclav)= lymphatic TB
  • bone/joint pain, back pain, joint swelling= joint or skeletal TB
  • abdo or pelvic pain, constip, bowel obstruct= GI TB
  • urinary symptoms (dysuria, haematuria, frequency)= GU TB
  • sterile pyuria= renal TB
  • headache, V, irritability, confusion, cranial nerve abnorm= TB meningitis
  • skin lesions= cutaneous TB

-SOB, chest pain, ankle swelling= TB pericarditis

  • occular inflam or visual disturbance= ocular TB (rare)
650
Q

Examples of skin lesions in cutaneous TB?

A

erythema nodosum (hypersensitivity reaction triggered by TB)

lupus vulgaris (painful nodular lesions affecting face)

651
Q

How may children present with TB?

A

non-specific

poor weight gain, faltering growth, fatigue, persistent fever

652
Q

CXR finding for active pulmonary TB?

A
  • bilateral hilar lymphadenopathy
  • upper lobe cavitation is classic of reactivated TB

NICE= cavitation; pleural effusion; mediastinal or hilar lymphadenopathy or parenchymal infiltrates mainly in the upper lobes

653
Q

Sputum samples for TB?

A

3, esp if CXR suggest TB

3 spontaneously produced, deep cough sputum samples; one early morning.
- for microscopy for acid-fasr bacilli(Ziehl-Neelsen stain), mycobacteria culture and specialist molecular test/drug sensitivity testing

654
Q

What Ix could you do if pt has suspected active extrapulmonary TB?

A

CXR + 3 sputum samples + either….

joint or spinal plain X-ray; abdo, renal tract or lymph node USS; early morning urine sample for dip, microscopy (sterile pyuria) and Mycobacteria culture; ECHO (pericarditis); CT chest, CNS or bone/joints, LP (CNS TB)

655
Q

False negative results for TB are more common in who?

A

children and the immunocompromised eg. HIV

656
Q

Screening for TB helps identify what?

A

latent TB

657
Q

The results of specialist screening tests to identify latent TB should be interpreted taking into account what?

A

immune status; Hx of exposure to TB and the BCG vaccine; other RFs

658
Q

Types of screening test for TB (latent)?

A

1) Mantoux test

2) Interferon-gamma release assay (IGRA) test

659
Q

Mantoux test used to screen for latent TB?

A

0.1ml of 1:1000 purified protein derivative Tuberculin is injected intradermally. Skin inspected for signs of local reaction (induration) after 2-3d.
+ve= induration of 5mm or more, regardless of previous BCG vaccine Hx.

Offered to children/young people 2-17yrs who gace been in close contact with pt with TB & new entrants to UK from high TB prevalence country.

<2yrs who are close contacts should be referred to specialist.

660
Q

Interferon-gamma release assay (IGRA) test for screening for latent TB?

A

Blood test= detects response of WBC to TB antigens.
Less likely to give false positive and gives rapid result.
<65yrs from under-served groups (eg. IVDU or homelessness) may be offered IGRA test.

661
Q

Who may be offered both Mantoux test and IGRA test to screen for latent TB?

A

severely immunocompromised at risk of TB

662
Q

What if latent TB screening test is +ve?

A

assessed for active TB

if no signs of active infective on basis of symptoms and CXR then treat for latent TB by local MD TB team to prevent progression to active disease

663
Q

Mx for latent TB?

A

3m of isoniazid (with pyridoxine) + rifampicin= <35yrs at low risk of hepatotoxicity

or

6m of isoniazid (with pyridoxine)= if rifamycin interactions may be concern (eg. pts with HIV or transplants)

664
Q

Is TB a notifiable disease?

A

yes, notify within 3 working days

notify a new culture confirmed case of TB or where TB is suspected and decision made to Tx pt

665
Q

Specialist assessment for TB?

A

Rapid diagnostic nucleic acid amplification tests (NAATs) for the Mycobacterium tuberculosis complex may be used on primary specimens if there is:
-clinical suspicion & HIV, or
- a rapid diagnosis needed or
- contact tracing of large numbers of people may be needed.

  • May need sputum induction, bronchoscopy and lavage, gastric aspiration; organ-specific aspiration or biopsy; or CT/MRI
666
Q

Mx for active TB?

A

6m isoniazid (with pyridoxine) + rifampicim AND in the 1st 2m: pyrazinamide + ethambutol

667
Q

How is TB Tx success defined?

A

by completion of therapy with negative follow-up sputum samples

668
Q

Pts with active TB of CNS require what?

A

prolonged Tx regimen
May also receive corticosteroids (dexa or pred) for 4-8w

669
Q

For TB, altered Tx regimens may be required in who?

A

pts with renal impairment (particularly ethambutol and pyrazinamide which are renally excreted)

670
Q

Mx for multidrug-resistant (MDR) TB?

A

prolonged Tx (18-24m) with at least 6 drugs to which Mycobacterium is likely sensitive

often less efficaious and more poorly tolerated due to increased adverse effects

671
Q

Who may be a candidate for surgical Mx of MDR TB?

A

pts with potentially resectable unilateral disease (or apical bilateral disease in selected cases) with adequate lung function who have not responded to medical Tx

672
Q

Differential diagnosis for active pulmonary TB?

A
  • viral URTI
  • asthma
  • chest infection
  • COPD
  • lung fibrosis
  • lung ca
  • pulmonary sarcoidosis (more of dry cough)
673
Q

Differential diagnosis for active extrapulmonary TB?

A
  • lymphoma
  • malignant pleural effusion
  • IBD
674
Q

Common side effects of TB Abx?

A

R.ifampicin= red urine, hepatitis

I.soniazid= peripheral neuropathy, hepatitis

P.yranzinamide= gout, rash, hepatitis

E.thambutol= optic neuritis

675
Q

Why do you give pyridoxine (vit B6) with isoniazid for TB?

A

S/E of isoniazid is peripheral neuropathy and so give it to prevent this

676
Q

What should you do before and during taking ethambutol for TB?

A

check visual acuity before and during Tx

677
Q

Are pts with latent TB infectious?

A

NO so no restrictions in terms of employment ect. unless becomes active

678
Q

RFs for developing active TB eg. if have latent?

A

silicosis
chronic renal failure
HIV positive
solid organ transplantation with immunosuppression
intravenous drug use
haematological malignancy
anti-TNF treatment
previous gastrectomy

679
Q

How are pts typically diagnosed with latent TB?

A

+ve tuberculin skin test (Mantoux test) or Interferon-Gamma Release Assay (IGRA) combined with a normal chest x-ray (which excludes active TB)

680
Q

Directly observed therapy 3x a week dosing regimen may be used in what groups of pts with TB?

A
  • homeless pts with active TB
  • pts who are likely to have poor concordance
  • all prisoners with active or latent TB
681
Q

Overall possible Cx of TB treatment?

A

Immune reconstitution disease= typically 3-6 after starting; presents with enlarging lymph nodes

682
Q

TB pathophysiology?

A

macrophages migrate to regional lymph nodes -> affected lymph codes + lung lesion= Ghon complex -> leads to formation of granuloma which is a collection of epithelioid histiocytes; presence of caseous necrosis in the centre

inflam response is mediated by type 4 hypersensitivity reaction

683
Q

What is Ghon complex in TB?

A

lung lesion + affected lymph nodes

684
Q

What is a granuloma in TB?

A

collection of epithelioid histiocytes

685
Q

TB in healthy individuals vs immunocompromised individuals?

A

healthy= TB may be contained

immunocompromised= disseminated (miliary TB) may occur

686
Q

What countries may be RFs for TB?

A

Asia, Latin America, Eastern Europe, Africa

687
Q

Examples of immunocompromised individuals that may have increased risk of TB?

A

diabetics, pts on immunosuppressive theraoy, malnourished or those with haematological malignancies

688
Q

Primary TB?

A

non-immune host exposed to M.TB may develop primary infection of lungs

Small lung lesion (Ghon focus) develops- composed of tubercle-laden macrophages.

Ghon focus + hilar lymph nodes= Ghon complex

Immunocompetent pts= inital lesion usually heals by fibrosis.
Immunocompromised- may develop disseminated disease (miliary TB)

689
Q

Secondary (post-primary) TB?

A

if host becomes immunocompromised the initial infection may become reactivated.

reactivation generally occurs in apex of lungs and may spread locally or to more distant sites

causes of immunocompromised= HIV, drugs eg. steroids, malnutrition

690
Q

Most common site for secondary TB?

A

lungs

691
Q

Extra-pulmonary infection in secondary TB examples?

A
  • CNS= TB meningitis (SERIOUS)
  • vertebral bodies (Pott’s disease)
  • Cervical lymph nodes= scrofuloderma
  • renal
  • GI
692
Q

Pott’s disease?

A

TB that has moved from lungs (pulmonary TB) to vertebral bodies in the spine (extra-pulmonary TB)

693
Q

CP of common cold?

A

mild, self-limiting, viral, URTI

nasal congestion, irritation, rhinorrhoea, sneezing, sore throat, cough after nasal symptoms clear; hoarse voice (associated largyngitis); malaise, headache

no known Tx improves time course of infection

694
Q

Most common cause of common cold?

A

Rhinovirus

695
Q

How long are people with common cold infectious?

A

several weeks

696
Q

Average number of common colds people get?

A

Adults= 2-3 per yr

Children= 5-8 (primary school or preschool)

697
Q

Cx of common cold?

A

sinusitis, LRTI, acute otitis media

secondary bacterial infection eg. pnuemonia

COPD or asthma exacerbations

young children/infants= viral wheeze, bronchiolitis, croup

698
Q

How long does common cold last?

A

acute
peak at 2-3d then decrease
around 1 week, cough can be up to 3w

younger children= lasts 10-14d

699
Q

Nasal discharge in common cold?

A

often profuse and clear at first then becomes thicker and darker as infection progresses

700
Q

Uncommon features of common cold?

A

fever, headache, myalgia, loss of taste & smell, eye irritability, feeling of pressure in ears or sinuses

701
Q

CP of common cold in young child?

A

Restlessness or irritability.
Nasal congestion, nasal discharge (rhinorrhoea), and sneezing. Severe nasal congestion may interfere with feeding, breathing, and sleep.
Cough. Occasionally, vomiting may follow a bout of coughing.
Fever.

702
Q

Mx for common cold?

A
  • adequate rest; normal activity won’t prolong illness
  • paracetamol or ibuprofen (if <5yrs only if has fever & distressed)
703
Q

What do URTIs involve?

A

mucosa of nasal cavity, sinuses, nasopharynx, oropharynx, larynx

704
Q

Causes of URTI?

A

Rhinovirus (most common)
Corona virus
Adenovirus
Influenza
Parainfluenza
RSV
Enterovirus

705
Q

Another name for URTI?

A

‘cold’
Coryzal symptoms

706
Q

Sings of UTRI?

A
  • erythema or injection at back of throat
  • nasal discharge
  • tender cervical lymphadenopathy
  • mild fever
707
Q

Criteria for assessment of URTI (common cold)?

A
  • <5yrs= NICE fever traffic light system
  • FeverPAIN score= likelihood of strep infection in adults with sore throat and guide decision making re Abx
708
Q

Boehaaves syndrome?

A

spontaneous rupture of oesophagus following repeated episodes of vomiting

distally sited and on L side

Hx of sudden onset severe chest pain that may complicate severe vomiting

severe sepsis occurs secondary to mediastinitis

709
Q

Diagnosis of Boerhaaves syndrome?

A

CT contrast swallow

710
Q

Tx for Boerhaaves syndrome?

A

thoracotomy and lavage

if <12hrs after onset= primary repair

> 12hrs= insertion of T tube to create controlled fistula between oesophagus and skin

> 24hrs= high mortality rate

711
Q

Angio-oedema?

A

swelling of deep dermis, subcut or submucosal tissue , often affecting face (lips, tongue and eyelids), genitalia, hands or feet.

Less common= submucosal swelling affecting bowel and airway

712
Q

Types of angio-oedema?

A
  • allergic
  • non-allergic drug reaction
  • hereditary angio-odema
  • acquired
  • idiopathic
713
Q

What usually causes acquired angio-oedema?

A

secondary to lymphoma or connective tissue disorder

714
Q

What usually causes non-allergic drug reaction angio-oedema?

A

ACE inhibitors

715
Q

Anaphylaxis?

A

severe, life-threatening, generalised or systemic hypersensitivity reaction characterised by rapidly developing airway and/or breathing and/or circulation problems usually associated with skin and mucosal changes

716
Q

Pathophysiology of anaphylaxis and angio-oedema?

A

both invl. histamine and/or bradykinin

but in anaphylaxis the reaction is more marked, resulting in an increase in vascular permeability and subsequent circulatory collapse

717
Q

Diagnosis of angio-oedema?

A

clinical

Ix may be used to identify associated condition, tirgger or exclude differential

718
Q

Approach to recognise and manage amnaphylaxis?

A

ABCDE

719
Q

Mx for pt with rapidly developing angio-oedema without anaphlaxis?

A

Slow IV or IM chlorphenamine and hydrocortisone + emergency admission

720
Q

Mx for pt with stable angio-oedema without anaphylaxis?

A
  • identify and remove underlying cause
  • non-sedating antihistamine (cetirizine up to 6w)
  • severe= + oral corticosteroid (pred 40mg od up to 7d)
  • refer to immuno or derm if cause is not identifiable or avoidable
721
Q

Mx for anaphylaxis?

A

1) unresponsive and not breathing= CPR

2) IM adrenaline 1:1000

3) assess response after 5mins

4) repeat adrenaline dose if no improvement

5) no improvement after 2 doses= IM adrenaline every 5mins until adequate response

Also give high flow O2, IV fluid challenge (if hypotension, shock or no initial response) and monitor pulse, O2 sats, BP and ECG.
- Consider inhaled salbutamol or ipratropium if wheezy

722
Q

Position to put pt in anaphylaxis?

A

pt with airway and breathing problems may prefer to sit up

low BP= lie flat with or without leg elevation helpful

breathing and unconscious= recovery position

pregnant= lie on left side to prevent caval compression (inferior vena cava)

723
Q

Mx following emergency treatment for anaphylaxis?

A
  • refer to specialist allergy service
  • give 2 adrenaline auto-injectors as interim measures before their allergy appointment (instruct how and when to use)
724
Q

General clinical features of angio-oedema?

A
  • surface of skin may be normal or may be weals or other rashes
  • skin swelling less defined than in urticaria and can affect eyes, lips, genitalia, hands and/or feet
  • swelling often more painful than itchy and can take up to 72hrs to resolve
  • may be resp symptoms (stridor, wheeze or SOB) or gins of circulatory collapse= if present then consider anaphylaxis
725
Q

When to suspect idiopathic angio-oedema?

A

recurrent episodes of angio-oedema & urticaria and allergic cause can’t be identified

more common in autoimmune disorders eg. SLE and autoimmune thyroiditits

consider CRP, ESR, autoantibody screen and thyroid autoantibodies

refer to immuno or derm if suspected

726
Q

Angio-odema without urticaria?

A

non-allergic cause likely eg. non-allergic drug reaction; hereditary angio-odema (HAE) or acquired angio-oedema (AA)

727
Q

When to suspect hereditary angio-oedema (HAE)?

A

Hx of parent affected

presents after puberty

recurrent oedema of limbs, trunk, face, genitals

swelling (non-itchy, non-pitting, painless) take 24hrs to peak usually and resolve over 48-72hrs+

GI symptoms common (can mimic acute abdo); upper airway swelling less common

if suspect refer to immuno or derm

728
Q

How is diagnosis of HAE confirmed?

A

low serum levels of complement C1 inhibitor in pt with FHx of angio-oedema

729
Q

How is diagnosis of acquired angio-oedema confirmed?

A

low serum levels of complement C1 inhibitor in pt with known cause for the condition (eg. lymphoma= splenic villous lymphoma; or connective tissue disorder eg. SLE)

730
Q

Anaphylaxis is likely when what 3 criteria are met?

A

1) Sudden onset and rapid progression of symptoms

2) Life-threatening Airway and/or Breathing and/or Circulation problems

3) Skin and mucosal changes

731
Q

Onset of anaphylaxis?

A

several mins (acute)

feel and look unwell

anxious and can experience ‘sense of impending doom’

IV fasted trigger then stings then oral ingested trigger

732
Q

Airway problems in anaphylaxis?

A
  • airway swelling (throat and tongue swelling= pharyngeal/laryngeal oedema)
  • difficulty breathing and swallowing= feeling throat closing up
  • hoarse voice
  • stridor
733
Q

Stridor?

A

high-pitch inspiratory noise caused by upper airway obstruction

734
Q

Breathing problems in anaphylaxis?

A
  • SOB= increased RR
  • wheeze
  • tiredness
  • confusion= due to hypoxia
  • cyanosis (appear blue= late sign)
  • peripheral cap O2 sat <92%
  • resp arrest
735
Q

Respiratory arrest?

A

med emergency when stop breathing -> lack of O2 supply; needs immediate intervention to prevent brain damage or death

736
Q

Features of respiratory arrest?

A
  • cessation of breathing
  • hypoxia
  • no chest movement
  • loss of consciousness
737
Q

Causes of respiratory arrest?

A

1) Airway obstruction (e.g., choking, swelling, foreign objects).

2) Severe asthma or COPD exacerbation.

3) Drug overdose eg. opioids or sedatives.

4) Severe respiratory infections (e.g., pneumonia, COVID-19).

5) Head or neck injury that affects the brain’s control of breathing.

6) Neuromuscular disorders affecting respiratory muscles (e.g., Guillain-Barré syndrome, myasthenia gravis).

7) Severe allergic reactions (anaphylaxis).

738
Q

Mx of respiratory arrest?

A
  • Basic life support= open airway, rescue breaths and CPR is needed
  • Advanced life support= airway Mx (eg. intubation), mechanical ventilation and TUC (eg. reverse opioid overdose with naloxone)
739
Q

Circulatory problems in anaphylaxis?

A
  • signs of shock (pale, clammy)
  • tachycardia
  • low BP (faint, dizzy, collapse)
  • decreased level/loss of consciousness
  • cardiac arrest
  • can cause MI and ECG changes
740
Q

D part of A to E in anaphylaxis?

A

Disability

A, B & C can alter neuro status (D) due to decreased brain perfusion, confusion and agitation

741
Q

Skin and/or mucosal changes in anaphylaxis?

A

Exposure in A to E

Often first features, in over 80% of reactions and can be subtle or dramatic

May be erythema (patchy or generalised red rash), urticaria or angio-oedema

742
Q

Skin changes without life-threatening airway, brathing or circulation problems?

A

DO NOT signify anaphylactic reaction.

743
Q

Skin and mucosal changes can be subtle or absent in what percent of anaphylactic reactions?

A

20% (so be aware when looking at anaphylaxis criteria)

744
Q

Some people with anaphylaxis may only present with what?

A

decrease in BP (circulatory problem)

745
Q

What other symptoms apart from A,B & C and skin/mucosal changes may be present in anaphylaxis?

A

GI symptoms eg. vomiting, abdo pain and incontinence

746
Q

Biphasic anaphylactic reaction?

A

Occasionally can occur.
Life-threatening recurrence of symptoms of anaphylaxis after initial presentation; without re-exposure to trigger.
Infrequent so difficult to predict.

747
Q

What may increase or decrease risk of bisphasic reactions following anaphylaxis?

A

Less likely= food induced anaphylaxis

Increased risk= present with hypotension or idiopathic anaphylaxis

748
Q

When would a biphasic reaction following anaphylaxis occur?

A

hrs to days after initial; typically 1-72hrs following

749
Q

Why may a biphasic reaction occur following anaphylaxis?

A

1) ongoing release of inflam mediators eg. histamine, leukotrienes and prostaglandins and so can cause a delayed resurgence of symptoms

2) incomplete clearance of inflam mediators

3) insuff Tx: may have controlled symptoms but not have stopped immune response so reaction may flare up again once Tx worn off

4) severity and prolonged initial reaction

5) duration of allergen exposure before Tx (eg. ongoing ingestion of allergenic food) may cause prolonged immune response increasing risk of biphasic reaction

750
Q

Differential diagnosis of angio-oedema?

A
  • acute contact dermatitis
  • cellulitis
  • connective tissue disorders eg. SLE
  • erysipelas
  • idiopathic scrotal oedema in children
  • lymphoedema
  • Rosenthal-Melkersson syndrome
  • surgical abdomen
751
Q

Differential diagnosis of anaphylaxis?

A
  • angio-oedema
  • asthma
  • acute anxiety
  • breath-holding episode in a child
  • foreign body aspiration
  • hypoglycaemia
  • PE
  • urticaria
  • vasovagal episode
  • mastocytosis
  • carcinoid syndrome
  • scombroid poisoning (from contaminated fish)
  • seizure
  • septic shock
752
Q

What if it is likely for stable angio-oedema without anaphylaxis to be persistent or recurrent?

A

daily antihistamine 3-6m then review

If long Hx of urticaria & A-O then 6-12m

753
Q

Where to infection IM adrenaline for anaphylaxis?

A

anterolateral aspect of the middle third of thigh (ideally) or arm depending on access

754
Q

How to assess response to adrenaline during anaphylaxis?

A

RR, O2 sats, HR, BP, level of consciousness and auscultate for wheeze

755
Q

If possible, how to give O2 for anaphylaxis and what are the target sats?

A

highest conc possible asap using mask with oxygen reservoir

94-98% target sats (or 88-92% in pt at risk of hypercapnic resp failure)

756
Q

During Mx for anaphylaxis, what do you do in the presence of hypotension/shock or poor response to initial dose of adrenaline?

A

obtain IV access and give rapid IV bolus (Hartmann’s or normal saline) using 500-1000mL in adult or 10mL/kg in child.

more fluids can be given if needed

757
Q

What should you consider giving in the Mx of anaphylaxis if pt is wheezy (esp in pt with known asthma)?

A

inhaled salbutamol or ipratropium bromide

758
Q

Follow up for pt with anaphylaxis once discharged?

A
  • refer to specialist allergy service
  • provide 2 adrenaline auto-injectors before allergy appointment (carry at all times, check expiry dates)
759
Q

Advice to give pt if they have another anaphylactic reaction?

A
  • use one adrenaline auto-injector and call 999 even if symptoms improving
  • lie flat with legs raised to maintain blood flow; if breathing diff then sit up
  • use 2nd auto-injector if don’t feel better after 15mins after first
760
Q

A dose of adrenaline IM for anaphylaxis if >12yrs?

A

adrenaline (IM) 1:1000
500 micrograms (0.5mL)

761
Q

A dose of adrenaline IM for anaphylaxis if 6-12yrs?

A

adrenaline (IM) 1:1000
300 micrograms (0.3mL)

762
Q

A dose of adrenaline IM for anaphylaxis if 6m-6yrs?

A

adrenaline (IM) 1:1000
150 micrograms (0.15mL)

763
Q

A dose of adrenaline IM for anaphylaxis if younger than 6m?

A

adrenaline (IM) 1:1000
100-150 micrograms (0.1-0.15mL)

764
Q

Dose of chlorphenamine for anaphylaxis and angio-oedema?

A

slow IM or IV

> 12yrs= 10mg
6-12yrs= 5mg
6m-6yrs= 2.5mg
<6m= 250 ug/kg

765
Q

Dose of hydrocortisone for anaphylaxis and angio-oedema?

A

slow IM or IV

> 12yrs= 200mg
6-12yrs= 100mg
6m-6yrs= 50mg
<6m= 25mg

766
Q

Dose of nebulised salbutamol for anaphylaxis and angio-oedema?

A

> 12yrs= 5mg
6-12yrs= 5mg
6m-6yrs= 2.5mg
<6m= 2.5mg

767
Q

How to inject adrenaline for anaphylaxis?

A

25mm needle IM at 90 degrees to skin, skin stretched not bunched

768
Q

Example of adrenaline auto-injector given to pt for self-administration at first signs of anaphylaxis?

A

EpiPen Autoinjector 0.3mg

  • 300 micrograms (1 pen) inject then another 300 microgram pen after 5 mins
769
Q

What dose adrenaline 1:1000 500micrograms (0.5mg) mean?

A

0.5ml 1 in 1000 adrenalinew

770
Q

Discharge guidance following anaphylaxis?

A

1) Fast-track (2hrs after symptom resolution)
2) Minimum of 6hrs after resolution
3) Minimum of 12hrs after resolution

771
Q

When can pt be discharged 2hrs after symptoms resolve following anaphylaxis?

A
  • good response to single dose adrenaline
  • complete resolution of symptoms
  • been given auto-injector and trained how to use
  • adequate supervision following discharge
772
Q

When must pt be discharged min 6hrs after symptoms resolve following anaphylaxis?

A

2 doses of IM adrenaline needed or previous biphasic reaction

773
Q
A
774
Q

When must pt be discharged min 12hrs after symptoms resolve following anaphylaxis?

A
  • severe reaction needing >2 doses adrenaline
  • severe asthma
  • possibility of ongoing reaction eg. slow release meds
  • presents late at night
  • pt in areas where access to emergency care may be difficult
  • observation for 12hrs
774
Q

What can be used to determine whether a resp disease is obstructive or restrictive?

A

pulmonary function tests

775
Q

Signs of obstructive lung disease on pulmonary function tests?

A

FEV1= significantly reduced

FVC= reduced or normal

FEV1/FVC (FEV1%)= reduced

776
Q

Examples of obstructive lung disease?

A

asthma
COPD
bronchiectasis
bronchiolitis obliterans

777
Q

Signs of restrictive lung disease on pulmonary function tests?

A

FEV1= reduced

FVC= significantly reduced

FEV1/FVC (FEV1%)= normal or increased

778
Q

Examples of restrictive lung disease?

A

Pulmonary fibrosis
Asbestosis
Sarcoidosis
Acute respiratory distress syndrome
Infant respiratory distress syndrome
Kyphoscoliosis e.g. ankylosing spondylitis
Neuromuscular disorders
Severe obesity

779
Q
A
780
Q

Causes of haemoptysis?

A
  • lung ca
  • pulmonary oedema
  • TB
  • PE
  • LRTI
  • bronchiectasis
  • mitral stenosis
  • aspergilloma
  • Granulomatosis with polyangiitis
  • Goodpasture’s
781
Q

Short summary of pulmonary oedema signs/symptoms?

A

Dyspnoea

Bibasal crackles and S3 are the most reliable signs

Haemoptysis

782
Q

Short summary of TB signs/symptoms?

A

Fever, night sweats, anorexia, weight loss, haemoptysis

783
Q

Short summary of PE signs/symptoms?

A

Pleuritic chest pain
Tachycardia, tachypnoea, haemoptysis

784
Q

Short summary of LRTI signs/symptoms?

A

Usually acute history of purulent cough

785
Q

Short summary of bronchiectasis signs/symptoms?

A

Usually long history of cough and daily purulent sputum production

786
Q

Short summary of mitral stenosis signs/symptoms?

A

Dyspnoea
Atrial fibrillation
Malar flush on cheeks
Mid-diastolic murmur
Haemoptysis

787
Q

Short summary of Aspergilloma signs/symptoms?

A

Often past history of tuberculosis.
Haemoptysis may be severe
Chest x-ray shows rounded opacity

788
Q

Short summary of Granulomatosis with polyangiitis signs/symptoms?

A

Upper respiratory tract: epistaxis, sinusitis, nasal crusting
Lower respiratory tract: dyspnoea, haemoptysis
Glomerulonephritis
Saddle-shape nose deformity

789
Q

Short summary of Goodpasture’s signs/symptoms?

A

Haemoptysis
Systemically unwell: fever, nausea
Glomerulonephritis

790
Q

How can pleural effusions be classified?

A

transudate or exudate according to the protein concentration

791
Q

Transudate vs exudate pleural effusion?

A

Transudate= <30g/L protein

Exudate= >30g/L protein

792
Q

Causes of transudate pleural effusion?

A
  • Heart failure (most common)
  • Hypoalbuminaemia= liver disease, nephrotic syndrome, malabsorption
  • hypothyroidism
  • Meig’s syndrome
793
Q

Causes of exudate pleural effusion?

A
  • infection= pneumonia (most common); TB; subphrenic abscess
  • connective tissue disease= RA; SLE
  • neoplasia= lung ca; mesothelioma; metastases
  • pancreatitis
  • PE
  • Dressler’s
  • yellow nail syndrome
794
Q

CP of pleural effusion?

A
  • dyspnoea, non-productive cough, chest pain
  • dullness to percussion, reduced breath sounds and reduced chest expansion
795
Q

Transudate fluid eg. in pleural effusion?

A

Clear
Low protein (<30g/L)

Results from systemic factors that alter the balance of fluid movement across capillary membranes such as increased hydrostatic pressure or decreased oncotic pressure.

Causes of transudate= CHF, cirrhosis and nephrotic syndrome

796
Q

Exudate fluid eg. in pleural effusion?

A

Cloudy or turbid and high protein content (>30g/L)

Occurs due to local factors that increase permability of capillary membranes, often related to imflam, infection or malignancy.

Causes= infection (pneumonia), malignancy, inflam condicitons eg. rheumatoid arthritis

797
Q

Why is there a high protein content in exudate?

A

Exudate high= due to inflam, infection or injury to tissues -> causes blood vessels (capillary membranes) to become more permeable (leaky) -> increased permability means that fluid, protein and cells can pass through vessel wall into surrounding tissue/cavity (large molecules can escape)

798
Q

Why is there a low protein content in transudate?

A

Forms due to systemic imbalance in fluid dynamics rather than local inflam. These imbalances can be caused by:
- increased hydrostatic pressure (eg. in CHF)
or
- decreased oncotic pressure (eg. in hypoalbuminaemia)

Fluid is pushed out of blood vessels (capillary membrane) due to pressure changes but the vessel walls remain intact so only water and small solutes (like electrolytes) can escape; but proteins and larger molecules remain in bloodstream.

799
Q

Ix for pleural effusion?

A
  • posterioranterior (PA) CXR in all pts
  • Pleural aspiration using USS
  • can use contrast CT to Ix underlying cause, esp. for exudative effusions
800
Q

Pleural aspiration for pleural effusion?

A

21G needle and 50ml syringe
with USS
- send fluid for pH, protein, lactate dehydrogenase (LDH), cytology and microbio

801
Q

Criteria to distinguish between transudate and exudate in pleural effusion? (esp. in borderline cases)

A

Light’s criteria

802
Q

Light’s criteria to distinguish between transudate and exudate in pleural effusion? (esp. in borderline cases)

A

If protein level 25-35g/L, use Light’s criteria. Exudate likely if at least 1 of the following is met:

  • pleural fluid protein divided by serum protein >0.5
  • pleural fluid LDH divided by serum LDH >0.6
  • pleural fluid LDH more than 2/3rds the upper limits of normal serum LDH
803
Q

What may low glucose from fluid aspiration in pleural effusion suggest?

A

RA, TB

804
Q

What may raised amylase from fluid aspiration in pleural effusion suggest?

A

pancreatitis; oesophageal perforation

805
Q

What may heavy blood staining from fluid aspiration in pleural effusion suggest?

A

mesothelioma; PE; TB

806
Q

Pt with pleural effusion in association with sepsis or pneumonic illness require what?

A

diagnostic pleural fluid sampling

807
Q

Pt with pleural effusion + sepsis or pneumonic illness require diagnostic pleural fluid sampling. How does the result of this determine Mx?

A
  • fluid is purulent or turbid/cloudy= chest tube to allow drainage
  • fluid is clear but pH is <7.2 in pts with suspected pleural infection= chest tube
808
Q

Mx for recurrent pleural effusion?

A
  • recurrent aspiration
  • pleurodesis
  • indwelling pleural catheter
  • medical= eg. opioids to relieve dyspnoea

infection= ?chest drain is required following pleural fluid sampling

809
Q

Predisposing factors for obstructive sleep apnoea/hypopnoea syndrome?

A
  • obesity
  • macroglossia= acromegaly, hypothyroidism, amloidosis
  • large tonsils
  • Marfan’s
810
Q

CP of obstructive sleep apnoea/hypopnoea syndrome?

A

partner complains of XS snoring and may report periods of apnoea

811
Q

Consequence of obstructive sleep apnoea/hypopnoea syndrome?

A
  • daytime somnolence
  • compensated resp acidosis
  • HTN
812
Q

Assess sleepiness in obstructive sleep apnoea/hypopnoea syndrome?

A
  • Epworth Sleepiness Scale= questionnaire completed by pt +/- partner
  • Multiple Sleep Latency Test (MSLT)= measure time to fall asleep in dark room (using EEG criteria)
813
Q

Ix for obstructive sleep apnoea/hypopnoea syndrome?

A
  • Assess sleepiness
  • refer for diagnostic test= Sleep studies (polysomnography)
814
Q

Sleep studies (polysomnography) to diagnose obstructive sleep apnoea/hypopnoea syndrome?

A

monitor pulse oximetry at night or can do full polysomnography= EEG, resp airflow, pulse oximetry, thoraco-abdo movement and snoring

815
Q

Mx for obstructive sleep apnoea/hypopnoea syndrome?

A
  • weight loss

1st= CPAP for moderate/severe OSAHS
- not tolerated= intra-oral devices (eg. mandibular advancement)

inform DVLA is causing XS daytime sleepiness

816
Q

OSAHS? OSAS?

A

obstructive sleep apnoea/hypopnoea syndrome

OSAS= obstructive sleep apnoea syndrome

817
Q

Obstructive sleep apnoea/hypopnoea syndrome?

A

sleep-related breathing disorder characterized by recurrent episodes of complete or partial obstruction of the upper airway during sleep, causing apnoea (complete airflow obstruction with temporary absence or cessation of breathing) or hypopnoea (decreased airflow), respectively.

818
Q

Why does OSAHS occur?

A

due to XS collapsing forces around pharynx that exceed the decreased muscle tone during sleep

819
Q

RFs for OSAS?

A

age, male sex, obesity, family history of OSAS, nasopharyngeal obstruction (for example adenotonsillar hypertrophy), craniofacial abnormalities, neuromuscular disorders, and lifestyle factors (such as smoking, alcohol, and sleeping supine).

820
Q

Child with OSAS?

A
  • refer ENT if there is nasopharyngeal obstruction and snoring at night.
  • paediatrician if there is a congenital or developmental disorder, associated condition, or obesity contributing to symptoms.
821
Q

A1AT stands for?

A

alpha-1 antitrypsin def

822
Q

Alpha-1 antitrypsin def (A1AT)?

A

common inherited condition caused by lack of protease inhibitor (Pi) normally produced by liver

classically causes emphysema (i.e COPD) in pts who are young and non-smokers

823
Q

COPD in young pt who are non-smokers (may have liver cirrhosis/ hepatocellular carcinoma in adults of cholestasis in children)?

A

think A1AT def

824
Q

Role of A1AT?

A

protect cells from enzymes such as neutrophil elastase

825
Q

A1AT def genetic inheritance?

A

A1AT located on chromosome 14

autosomal recessive/co-dominant

826
Q

A1AT def alleles?

A

alleles classified by electrophoretic mobility= M is normal, S for slow, Z for very slow

Normal= PiMM
Heterozygous= PiMZ

Homozygous PiSS= 50% normal A1AT levels
Homozygous PiZZ= 10% normal A1AT levels

827
Q

Features of A1AT def?

A
  • pt who manifest disease usually PiZZ genotype
  • lungs= panacinar emphysema, most marked in lower lobes
  • liver= cirrhosis and hepatocellular carcinoma in adults, cholestasis in children
828
Q

Ix for A1AT def?

A
  • A1AT conc
  • spirometry- obstructive
829
Q

Mx for A1AT def?

A
  • no smoking
  • supportive= bronchodilators, physiotheraoy
  • IV AT1T protein concentrates
  • surgery= lung volume reduction surgery, lung transplant
830
Q

Allergic bronchopulmonary asperigillosis?

A

results from allergy to Aspergillus spores

831
Q

Hx of bronchiectasis and eosinophilia?

A

allergic bronchopulmonary aspergillosis

832
Q

Features of allergic bronchopulmonary aspergillosis?

A

bronchoconstriction= wheeze, cough, dyspnoea; may have previous label of asthma

bronchiectasis (proximal)

833
Q

Ix for allergic bronchopulmonary aspergillosis?

A
  • eosinophilia
  • flitting CXR changes
  • positive radioallergosorbent (RAST) test to Aspergillus
  • positive IgG precipitins (not as positive as in aspergilloma)
  • raised IgE
834
Q

Mx of allergic bronchopulmonary aspergillosis?

A

Oral glucocorticoids

2nd line= itraconazole

835
Q

3 types of altitude related disorders?

A

1) acute mountain sickness (AMS)

may progress to…
2) high altitude pulmonary oedema (HAPE) or
3) high altitude cerebral oedema (HACE)

836
Q

What are AMS, HAPE and HACE (altitude related disorders) all due do?

A

chronic hypobaric hypoxia which develops at high altitudes

837
Q

Acute mountain sickness features?

A
  • self-limiting
  • headache
  • nausea
  • fatigue
838
Q

When do features of AMS start to occur and how long do they last?

A

above 2500-3000m
develop gradually over 6-12hrs and can last a number of days

839
Q

Prevention of AMS?

A
  • risk may be correlated to physical fitness
  • gain altitude of no more than 500m a day
  • acetazolamide
840
Q

What is acetazolamide?

A

a carbonic anhydrase inhibitor used to prevent AMS

causes primary metabolic acidosis and compensatory resp alkalosis which increases RR and improves oxygenation

841
Q

Treatment of AMS?

A

descent

842
Q

Pt with AMS may develop HAPE or HACE (potentially fatal) when?

A

if go above 4000m (minority of people will go on to develop this)

843
Q

Presentation of HAPE (high altitude pulmonary oedema)?

A

classic pulmonary oedema features

844
Q

Mechanism of HAPE (high altitude pulmonary oedema)?

A

hypobaric hypoxia → uneven hypoxic pulmonary vasoconstriction → uneven blood flow in the lungs → areas of the lung receiving more blood experience an increase in capillary pressure → more fluid leakage. Hypoxia may also directly increase capillary permeability, exacerbating fluid leakage into the alveolar space.

845
Q

Features of HACE (high altitude cerebral oedema)?

A

headache, ataxia, papilloedema

846
Q

Mechanism of HACE (high altitude cerebral oedema)?

A

in contrast to HAPE, cerebral vasodilation is the problem. Hypoxia → cerebral vasodilation → elevated cerebral blood volume

also, hypoxia → increase in the permeability of the blood-brain barrier → capillaries in the brain more leaky → leading to fluid accumulation in the extracellular spaces
both these factors → cerebral oedema

847
Q

Mx of HACE (high altitude cerebral oedema)?

A

descent and dexamethasone

848
Q

Mx of HAPE (high altitude pulmonary oedema)?

A

descent; O2 if available and medication= nifedipine, dexa, acetazolamide, or phosphodiesterase type V inhibitors (all reduce systolic pulmon artery pressure)

849
Q

5 steps for ABG interpretation?

A

1) How is the pt?

2) Is the pt hypoxaemic? (<10kPa)

3) Is the pt acidaemic (pH <7.35) or alkalaemic (pH >7.45)?

4) Respiratory component= what has happened to PaCO2? (resp acidosis/alkalosis or resp compensation)

5) Metabolic component= what is the bicarb level/base excess? (metabolic acidosis/alkalosis or renal compensation)

850
Q

ABG: step 2- how to know if pt is hypoxaemic?

A

the PaO2 on air should be >10kPa if normal

851
Q

ABG: step 3- how to know if pt is acidaemic or alkalaemic?

A

Acidaemic= pH <7.35

Alkalaemic= pH >7.45

852
Q

ABG: step 4- how to work out the respiratory component?

A

What has happened to PaCO2.

  • PaCO2 >6.0kPa= resp acidosis (or resp compensation for metabolic alkalosis)
  • PaCO2 <4.7kPa= resp alkalosis (or resp compensation for metabolic acidosis)
853
Q

ABG: step5- how to work out the respiratory component?

A

What is the bicarb/base excess.

  • Bicarb <22mmol/l (or base excess < -2mmol/l)= metabolic acidosis (or renal compensation for resp alkalosis)
  • Bicarb >26 (or base excess > +2)= metabolic alkalosis (or renal compensation for resp acidosis)
854
Q

ABG: PaCO2 > 6.0 kPa?

A

respiratory acidosis (or respiratory compensation for a metabolic alkalosis)

855
Q

ABG: PaCO2 < 4.7 kPa?

A

respiratory alkalosis (or respiratory compensation for a metabolic acidosis)

856
Q

ABG: bicarbonate < 22 mmol/l (or a base excess < - 2mmol/l)?

A

metabolic acidosis (or renal compensation for a respiratory alkalosis)

857
Q

ABG: bicarbonate > 26 mmol/l (or a base excess > + 2mmol/l)?

A

metabolic alkalosis (or renal compensation for a respiratory acidosis)

858
Q

ABG: low pH and high PaCO2?

A

resp acidosis

859
Q

ABG: high pH and low PaCO2?

A

resp alkalosis

860
Q

ABG: low pH and low bicarb?

A

metabolic acidosis

861
Q

ABG: high pH and high bicarb?

A

metabolic alkalosis

862
Q

ABG: way to remember resp/met acidosis/alkalosis results?

A

ROME

Respiratory = Opposite
low pH + high PaCO2 i.e. acidosis, or
high pH + low PaCO2 i.e. alkalosis

Metabolic = Equal
low pH + low bicarbonate i.e. acidosis, or
high pH + high bicarbonate i.e. akalosis

863
Q

ABG: resp acidosis vs alkalosis reading?

A

Acidosis= PaCO2 > 6.0 kPa (HIGH) and pH <7.35 (LOW)

Alkalosis= PaCO2 < 4.7 kPa (LOW) and pH >7.45 (HIGH)

864
Q

ABG: metabolic acidosis vs alkalosis reading?

A

Acidosis= bicarb <22 (or base excess <-2) (LOW) and pH <7.35 (LOW)

Alkalosis= bicarb >26 (or base excess >+2) (HIGH) and pH >7.45 (HIGH)

865
Q

ABG: what could resp acidosis or alkalosis also mean?

A

Resp acidosis or could be resp compensation for a metabolic alkalosis.

Resp alkalosis or could be resp compensation for metabolic acidosis.

866
Q

ABG: what could metabolic acidosis or alkalosis also mean?

A

Met acidosis or could be renal compensation for resp alkalosis.

Met alkalosis or could be renal compensation for resp acidosis.

867
Q

ABG: how to determine if there if compensation?

A

1) identify if primary issue is acidosis or alkalosis

2) check if HCO3- is moving in same direction as pH to indicate compensation

3) if pH is normal then there is complete compensation

868
Q

What does compensation mean in ABG?

A

body’s attempt to restore normal pH through changes in resp or metabolic function

869
Q

ABG: respiratory compensation explained?

A

Changes in PaCO2 levels through changes in ventilation. Fast.

eg. Metabolic acidosis low pH, low bicarb) then with compensation there is increase in ventilation to get rid of CO2 to raise pH (so low PaCO2)

870
Q

Example of ABG result showing metabolic acidosis with resp compensation?

A

pH LOW
bicarb LOW
PaCO2 LOW (due to hyperventilation)

871
Q

ABG: metabolic compensation explained?

A

Changes in bicarb through renal function. Longer-hrs to days.

eg. Resp acidosis (low pH, high PaCO2) then with compensation the kidneys retain bicarb to increase levels to increase pH (so high bicarb)

872
Q

Example of ABG result showing resp acidosis with metabolic compensation?

A

pH LOW
PaCO2 HIGH (hypoventilation)
Bicarb HIGH

873
Q

ABG results that mean if there is compensation?

A

In resp acidosis: compensation if high bicarb to increase pH.

Resp alkalosis: compensation if low bicarb to decrease pH.

Met acidosis: compensation if PaCO2 low to increase pH (due to hyperventilation)

Met alkalosis: compensation if PaCO2 high to increase pH (due to decrease pH)

874
Q

Aspiration pneumonia?

A

pnuemonia that develops as a result of forgein materials gaining entry to bronchial tree; eg. food or saliva

875
Q

What can develop as a result of aspiration pneumonia?

A

chemical pneumonitis depending on acidity of the aspirate; bacterial pathogens can add to the inflam

876
Q

Causes of aspiration pneumonia?

A

incompetent swallowing mechanism eg. due to neuro diease/injury= stroke, MS, intoxication.
Iatrogenic= intubation

877
Q

RFs for aspiration pneumonia?

A
  • poor dental hygiene
  • swallowing difficulties
  • prolonged hospitalisation or surgical procedures
  • impaired consciousness
  • impaired mucociliary clearance
878
Q

Most common site affected in aspiration pneumonia and why?

A

Right middle and lower lung lobes due to larger calibre and more vertical orientation of R main bronchus

879
Q

Examples of aerobic bacteria implicated in aspiration pneumonia?

A
  • strep pneumoniae
  • staph aureus
  • H.influenzae
  • p. aeruginosa
  • Klebsiella
880
Q

Aerobic bacteria often seen in aspiration lobar pneumonia in alcoholics?

A

Klebsiella

881
Q

Anaerobic bacteria implicated in aspiration pneumonia?

A
  • bacterioides
  • prevotella
  • fusobacterium
  • peptosteptococcus
882
Q

Common postop Cx where basal alveolar collapse and lead to resp difficulty?

A

atelectasis

883
Q

What causes atelectasis?

A

when airways become obstructed by bronchial secretions

884
Q

Features of atelectasis?

A

suspected in presentation of dyspnoea and hypoxaemia around 72hrs post op

885
Q

Suspect what if pt has dyspnoea and hypoxaemia around 72hrs post op?

A

atelectasis

886
Q

Mx of atelectasis?

A
  • position pt upright
  • chest physio: breathing exercises
887
Q

Causes of bilateral hilar lymphadenopathy?

A

Most common= TB and sarcodiosis

  • lymphoma/malignancy
  • pneumoconiosis eg. berylliosis
  • fungi eg. histoplasmosis, coccidiodomycosis
888
Q

What is bilateral hilar lymphadenopathy?

A

bilateral enlargement of the lymph nodes of pulmonary hila

889
Q

What is a chest drain?

A

tube inserted into pleural cavity which creates a one-way valve, allowing movement of air or liquid out the cavity

890
Q

Indications of chest drain?

A
  • pleural effusion
  • pneumothorax (not for conservative Mx or aspiration)
  • empyema
  • haemothorax
  • haemopnuemothorax
  • chylothorax
  • sometimes in penetrating chest wall injury in ventilated pts
891
Q

Contraindications for chest drain (except resp compromise in emergency then assess on individual case basis)?

A
  • INR >1.3
  • platelet count <75
  • pulmonary bullae
  • pleural adhesions
892
Q

Steps to insert chest drain?

A

1) consent and imaging
2) supine position or at 45º angle
3) forearm behind head for easy access to axilla
4) 5th ICS mid axillary line; use USS in all cases of fluid within pleura
5) lidocaine (up to 3mg/kg) injection
6) insert tube using seldinger technique
7) secure with straight stitch or adhesive dressing

893
Q

How to confirm position of chest drain?

A

aspiration of fluid from drainage tubing, by ‘swinging’ of the fluid within the drain tubing when pt inspires and on CXR

894
Q

Cx of chest drain?

A
  • failure of insertion
  • bleeding (around site of drain or into pleural space)
  • infection
  • penetration of lung
  • re-expansion pulmonary oedema
895
Q

What if there is failure of insertion of chest drain?

A

drain may be abutting the apical pleura, in which case it should be pulled back, or may be subcutaneous or in rare cases could enter the abdominal cavity. In both latter cases, the drain should be removed and re-sited.

896
Q

Cx of chest drain: re-expansion pulmonary oedema?

A

onset of cough and/or SOB

if suspect, clamp chest drain and emergency CXR

to avoid= clamp the drain tubing regularly in the event of rapid fluid output ie. drain output should not exceed 1L of fluid over <6hrs

897
Q

Removal of chest drain depends upon initial indication, eg?

A
  • fluid drainage from pleural cavity= remove when no output for >24hrs and imaging shows resolution
  • pneumothorax= remove when no longer bubbling spontaneously or when pt coughs and ideally when imaging shows resolution
  • penetrating injury= review by specialist
898
Q

Anatomy of insertion for chest drain?

A

‘safe triangle’

mid axillary line of 5th ICS; bordered by: Anterior edge latissimus dorsi, the lateral border of pectoralis major, a line superior to the horizontal level of the nipple, and the apex below the axilla.

899
Q

Another anatomical site for insertion of chest drain?

A

triangle of auscultation

behind the scapula. It is bounded above by the trapezius, below by the latissimus dorsi, and laterally by the vertebral border of the scapula; the floor is partly formed by the rhomboid major. If the scapula is drawn forward by folding the arms across the chest, and the trunk bent forward, parts of the sixth and seventh ribs and the interspace between them become subcutaneous and available for auscultation

900
Q

Causes of clubbing can be grouped into what?

A

cardiac, resp and other

901
Q

Cardiac causes of clubbing?

A

cyanotic congenital heart disease (Fallot’s, TGA)

bacterial endocarditis

atrial myxoma

902
Q

Resp causes of clubbing?

A
  • lung ca
  • pyogenic conditions: CF, bronchiectasis, abscess, empyema
  • TB
  • asbestosis, mesothelioma
  • fibrosing alveolitis
903
Q

Other causes of clubbing?

A
  • Crohn’s, to lesser extent UC
  • cirrhosis, primary biliary cirrhosis
  • Graves (thyroid acropachy)
  • rare: Whipple’s disease
904
Q

Another name for eosinophilic granulmatosis with polyangiitis (EGPA)?

A

Churg-Strauss syndrome

905
Q

What is eosinophilic granulmatosis with polyangiitis (EGPA)?

A

an ANCA associated small-medium vessel vasculitis?

906
Q

Features of eosinophilic granulmatosis with polyangiitis (EGPA)?

A
  • asthma
  • blood eosinophilia (eg >10%)
  • paranasal sinusitis
  • mononeuritis multiplex
  • pANCA positive in 60%
907
Q

Granulomatosis with polyangiitis (Wegener’s granulomatosis) vs Churg-Strauss syndrome (eosinophilic granulmatosis with polyangiitis)?

A

Wegener’s= renal failure; epistaxis/haemoptysis; cANCA

Churg= asthma; pANCA; eosinophilia

Both= vasculitis; sinusitis; dyspnoea

908
Q

What may precipitate eosinophilic granulmatosis with polyangiitis (EGPA)?

A

leukotriene receptor antagonists (LTRA)

909
Q

Another name for extrinsic allergic alveolitis? (EAA)

A

hypersensitivity pneumonitis

910
Q

What is extrinsic allergic alveolitis (hypersensitivity pneumonitis)?

A

condition caused by hypersensitivity induced lung damage due to variety of inhaled organic particles

911
Q

What is though to cause extrinsic allergic alveolitis (hypersensitivity pneumonitis)?

A

immune-complex mediated tissue damage (type III hypersensitivity) although delayed hypersensitivity (type IV) thought to play a role, esp in chronic phase

912
Q

Examples of extrinsic allergic alveolitis (hypersensitivity pneumonitis)?

A
  • bird fancier’s lung
  • farmers lung
  • malt workers lung
  • mushroom worker’s lung
913
Q

Example of extrinsic allergic alveolitis (hypersensitivity pneumonitis): what causes bird fancier’s lung?

A

avian proteins from bird droppings

914
Q

Example of extrinsic allergic alveolitis (hypersensitivity pneumonitis): what causes farmers lung?

A

spores of Saccharopolyspora rectivirgula from wet hay (formerly Micropolyspora faeni)

915
Q

Example of extrinsic allergic alveolitis (hypersensitivity pneumonitis): what causes malt worker’s lung?

A

Aspergillus clavatus

916
Q

Example of extrinsic allergic alveolitis (hypersensitivity pneumonitis): what causes mushroom worker’s lung?

A

thermophulic actinomycetes

917
Q

Presentation of extrinsic allergic alveolitis (hypersensitivity pneumonitis)?

A

acute (4-8hrs after exposure):
- dyspnoea
- dry cough
- fever

chronic (occurs w-m after exposure):
- lethargy
- dyspnoea
- productive cough
- anorexia and weight loss

918
Q

Ix for extrinsic allergic alveolitis (hypersensitivity pneumonitis)?

A
  • imaging= upper/mid-zone fibrosis
  • bronchoalveolar lavage= lymphocytosis
  • serologic assays for specific IgG antibodies
  • blood= NO eosinophilia
919
Q

Mx for extrinsic allergic alveolitis (hypersensitivity pneumonitis)?

A
  • avoid precipitating factors
  • oral glucocorticoids
920
Q

Another name for granulomatosis with polyangiitis?

A

Wegener’s granulomatosis

921
Q

Granulomatosis with polyangiitis?

A

autoimmune condition associated with necrotising granulomatous vasculitis affecting both upper and lower resp tract and the kidneys

922
Q

Features of granulmatosis with polyangiitis?

A
  • URT= epistaxis, sinusitis, nasal crusting
  • LRT= dyspnoea, haemoptysis
  • rapidly progressive glomerulonephritis (‘pauci-immune’, 80%)
  • saddle-shaped nose deformity
  • vasculitic rash, eye invl. (eg. proptosis), cranial nerve lesions
923
Q

Ix for granulomatosis with polyangiitis?

A
  • cANCA +ve in >905, pANCA +ve in 25%
  • CXR= wide variety of presentations, incl. cavitating lesions
  • renal biopsy= epithelial crescents in Bowman’s capsule
924
Q

Mx of granulomatosis with polyangiitis?

A
  • steroids
  • cyclophosphamide (90% response)
  • plasma exchange
  • median survival= 8-9yrs
925
Q

Inhaler technique?

A

1) remove cap & shake

2) breathe out gently

3) put mouthpiece in mouth & as you begin to breathe in deep and slow, press the canister down and continue to inhale steadily and deeply

4) hold breath for 10secs or as long as comfortable

5) for a second dose wait for approx 30secs before repeating

only use device for number of doses on label then start new inhaler

926
Q

Kartagener’s syndrome (primary ciliary dyskinesia)?

A

rare autosomal recessive genetic ciliary disorder

triad= situs inversus, chronic sinusitis and bronchiectasis

most frequently occus in examinations due to its association with dextrocardia (eg. quiet heart sounds, small volume complexes in lateral leads)

927
Q

Kartagner’s syndrome (primary ciliary dyskinesia) pathogenesis?

A

dynein arm defect results in immotile cilia

928
Q

Features of kartagener’s syndrome (primary ciliary dyskinesia)?

A
  • dextrocardia or complete situs inversus
  • bronchiectasis
  • recurrent sinusitis
  • subfertility (secondary to diminished sperm motility and defective ciliary action in the fallopian tubes)
929
Q

What is Klebsiella pneumoniae?

A

gram-negative rod part of the normal gut flora

930
Q

What can Klebsiella pneumoniae cause?

A

pneumonia (typically following aspiration) and UTI

931
Q

‘red-current jelly’ sputum?

A

Klebsiella pneumonia

932
Q

Features of Klebsiella pneumonia?

A
  • more common in alcoholics and diabetics
  • may occur following aspiration
  • red-current jelly sputum
  • often affects upper lobes
933
Q

Prognosis of Klebsiella pneumoniae?

A
  • commonly causes lung abscess formation and empyema
  • mortality 30-50%
934
Q

Lung abscess?

A

well-circumscribed infection within lung parenchyma

935
Q

Lung abscess most commonly forms secondary to what?

A

aspiration pneumonia (RFs: poor dental hygiene, previous stroke, reduced consciousness)

936
Q

Causes of lung abscess?

A
  • secondary to aspiration pneumonia
  • haematogenous spread (eg. secondary to infective endocarditis)
  • direct extension (eg. from an empyema)
  • bronchial obstruction (eg. secondary from a lung tumour)
937
Q

Lung abscess’s are typically polymicrobial. What are some monomicrobial causes?

A
  • staph. aureus
  • Klebsiella pneumoniae
  • Pseudomonas aeruginosa
938
Q

Features of lung abscess?

A
  • similar to pneumonia but more subacute presentation: may develop over weeks
  • may see systemic features eg. night sweats and weight loss
  • fever
  • productive cough= foul-smelling sputum, haemoptysis in minority
  • chest pain
  • dyspnoea
939
Q

Signs of lung abscess?

A
  • dull percussion and bronchial breathing
  • may see clubbing
940
Q

Ix for lung abscess?

A
  • CXR= fluid filled space within area of consolidation; an air-fluid level is typically seen
  • sputum and blood cultures also
941
Q

Lung abscess Mx?

A
  • IV Abx
  • not resolving then percutaneous drainage may be needed or in v. rare cases surgical resection
942
Q

Mediastinum?

A

region between the pulmonary cavities

943
Q

What is the mediastinum covered by?

A

mediastinal pleura

944
Q

Where is the mediastinum?

A

between the pulmonary cavities and extends from the thoracic inlet superiorly to the diaphragm inferiorly

945
Q

Mediastinal regions?

A

Superior mediastinum (between manubriosternal angle and T4/5)

Middle mediastinum

Posterior mediastinum

Anterior mediastinum

946
Q

Contents of the superior mediastinum?

A

Superior vena cava
Brachiocephalic veins
Arch of aorta
Thoracic duct
Trachea
Oesophagus
Thymus
Vagus nerve
Left recurrent laryngeal nerve
Phrenic nerve

947
Q

Contents of the anterior mediastinum?

A

Thymic remnants
Lymph nodes
Fat

948
Q

Contents of the middle mediastinum?

A

Pericardium
Heart
Aortic root
Arch of azygos vein
Main bronchi

949
Q

Contents of the posterior mediastinum?

A

Oesophagus
Thoracic aorta
Azygos vein
Thoracic duct
Vagus nerve
Sympathetic nerve trunks
Splanchnic nerves

950
Q

Microscopic polyangiitis?

A

small vessel ANCA vasculitis

951
Q

Features of microscopic polyangiitis?

A
  • renal impairment= raised creatinine, haematuria, proteinuria
  • fever
  • lethargy, myalgia, weight loss
  • palpable purpura rash
  • cough, dyspnoea, haemoptysis
  • mononeuritis multiplex
952
Q

Ix for microscopic polyangiitis?

A
  • pANCA (against MPO)= +ve in 50-75%
  • cANCA (against PR3)= +ve in 40%
953
Q

Polyangiitis?

A

inflam of multiple types of vessels such as small arteries and veins

954
Q

Indications for non-invasive ventilation? (NIV)

A
  • COPD with resp acidosis pH 7.25-7.35
  • T2RF secondary to chest wall deformity, neuromuscular disease or obstructive sleep apnoea
  • cardiogenic pulmonary oedema unresponsive to CPAP
  • weaning from tracheal intubation
955
Q

Can NIV be used in COPD with resp acidosis in pts who are more acidotic eg. pH <7.25?

A

yes but need greater degree of monitoring eg. HDU and a lower threshold for intubation and ventilation should be used

956
Q

Recommended initial settings for bi-level pressure (BiPAP) support in COPD?

A
  • Expiratory Positive Airway Pressure (EPAP)= 4-5cm H2O
  • Inspiratory Positive Airway Pressure (IPAP): 12-15cm H2O
  • back up rate= 15 breaths/min
  • back up inspiration:expiration ratio= 1:3
957
Q

2 common types of non-invasive ventilation?

A

BiPAP (Bilevel Positive Airway Pressure) and CPAP (Continuous Positive Airway Pressure)

958
Q

BiPAP vs CPAP (NIV)?

A

BiPAP= provides 2 levels of pressure (IPAP and EPAP); more comfortable as easier to exhale due to lower EPAP setting; more expensive as more complex (2 pressure settings); more flexible as can adjust pressures for both inhalation and exhalation; more severe conditions or if don’t respond to CPAP

CPAP= continuous constant pressure throughout entire breathing process; pressure is set at fixed level to prevent airway collapse; 1st line for OSA when it is mild-moderate; exhaling against constant pressure uncomfortable so long-term use difficult; cheaper

959
Q

Why is the pressure in CPAP set at a fixed level?

A

to prevent airway collapse

960
Q

When to use CPAP vs BiPAP?

A

BiPAP= higher pressure needs; central sleep apnea; chronic resp conditions eg. COPD (due to additional support); restrictive lung disease/hypoventilation syndrome; acute resp distress or resp failure; CHF (more complex breathing patterns)

CPAP= OSA; milder breathing issues and lower pressure needs (don’t need more complex airway support); post-surgery or during recovery to maintain airway stability

961
Q

What does the oxygen dissociation curve describe?

A

relationship between % of sat Hb and partial pressure of O2 in blood; NOT affected by Hb conc

962
Q

Why does O2 dissociation curve shift to the left?

A

Lower oxygen delivery
eg. due to

HbF, methaemoglobin, carboxyhaemoglobin
Low [H+] (alkali)
Low pCO2
Low 2,3-DPG
Low temperature

963
Q

Why does O2 dissociation curve shift to the right?

A

Raised O2 delivery
eg. due to

Raised [H+] (acidic)
Raised pCO2
Raised 2,3-DPG
Raised temperature

964
Q

What is the L rule for the O2 dissociation curve?

A

Shifts to L → Lower oxygen delivery, caused by
Low [H+] (alkali)
Low pCO2
Low 2,3-DPG
Low temperature

Another mnemonic is ‘CADET, face Right!’ for CO2, Acid, 2,3-DPG, Exercise and Temperature

965
Q

What normally influences O2 affinity?

A

haemoglobin’s structural conformation, which is dependent on the heme component and globin chains. Normal adult haemoglobin (HbA) comprises two alpha and two beta chains.

966
Q

Structural alteration in Hb that may alter O2 affinity/variant Hb?

A
  • point mutations eg. HbS
  • changes in Heme affinity (Hb Kempsey (β99 Asp→Asn) showcases increased oxygen affinity, leading to impaired oxygen release in tissues.)
  • altered quaternary structure
  • changes in allosteric regulators (eg. 2,3-BPG, pH and CO2 levels) for example: Hb Rainier (β145 Tyr→His) shows reduced affinity for 2,3-BPG, leading to higher oxygen affinity and less efficient oxygen delivery to tissues.
  • Polymerisation eg. HbS polymerise under low O2 conditions, distorting RBCs and impairing O2 delivery
  • Aggregation of abnormal Hb can lead to haemolysis
967
Q

3 examples of clinical implications of variant Hb?

A

1) Polycythaemia= high O2-affinity variants may lead to tissue hypoxia and compensatory polycythaemia (can increase thrombotic risk so can Mx with low dose aspirin/ venesection)

2) cyanosis= Hb with reduced O2 affinity can cause cyanosis due to increased levels of deoxygenated Hb

3) Haemolytic anaemia= eg. sickle cell lead to chronic haemolytic anaemia

968
Q

Immediate Mx for pts who are critically ill (anaphylaxis, shock etc) as hypoxia kills?

A

Oxygen via non-rebreather (reservoir mask) at 15L/min

exclude certain conditions where pt is acutely unwell eg. MI but stable

969
Q

Oxygen sat targets?

A
  • acutely ill= 94-98%
  • risk of hypercapnia (eg. COPD pts)= 88-92%

O2 should be reduced in stable pts with satisfactory O2 sats

970
Q

O2 management in COPD pts?

A
  • prior to blood gas availability= 28% Venturi mask at 4L/min and aim for sats 88-92% (for pt with RF for hypercapnia but no prior history of resp acidosis)
  • adjust target range to 94-98% IF pCO2 NORMAL
971
Q

Situations where O2 therapy should not be routinely used if there is no evidence of hypoxia?

A
  • MI and ACS
  • stroke
  • obstetric emergnencies
  • anixety-related hyperventilation
972
Q

Psittacosis?

A

infection caused by Chlamydia psittaci; most common presentation is a cause of atypical pneumonia. Rare.

973
Q

When to suspect psittacosis?

A
  • typical fever + history of bird contact (84%)
  • or pneumonia with severe headache or organomegaly and failure to respond to penicillin Abx
  • more common in young adults
974
Q

What causes psiittacosis?

A

Chlamydia psittaci (obligate intracellular bacterium)

975
Q

Transmission of psittacosis?

A

typically from birds or bird secretions eg. urine and faeces, typically after cleaning bird cages

pet birds and wild birds

transmission from other animals or humans possible but very rare

976
Q

Presentation of psittacosis?

A

subacute onset of:

  • flu-like symptoms (90%)= fever, headache, myalgia
  • resp symptoms (82%)= dyspnoea, dry cough, chest pain
977
Q

Signs of psittacosis?

A
  • chest= unilateral crepitations and vesicular breathing (common), evidence of pleural effusion (uncommon)
  • abdo= hepatomegaly and splenomegaly (rare)
978
Q

Ix for psittacosis?

A
  • raised inflam markers
  • CXR= consolidation
  • confirmation with serology (usually part of atypical pneumonia screening)
979
Q

Mx of psittacosis?

A

1st line= tetracyclines e.g. doxycycline

2nd line= macrolides e.g. erythromycin

980
Q

Causes of resp acidosis?

A

COPD

decompensation in other respiratory conditions e.g. life-threatening asthma / pulmonary oedema

neuromuscular disease

obesity hypoventilation syndrome

sedative drugs: benzodiazepines, opiate overdose

981
Q

Causes of resp alkalosis?

A

anxiety leading to hyperventilation

pulmonary embolism

salicylate poisoning

CNS disorders: stroke, subarachnoid haemorrhage, encephalitis

altitude

pregnancy

982
Q

Salicylate overdose- does it lead to resp/met acidosis or alkalosis?

A

a mixed respiratory alkalosis and metabolic acidosis. Early stimulation of the respiratory centre leads to a respiratory alkalosis whilst later the direct acid effects of salicylates (combined with acute renal failure) may lead to an acidosis

983
Q
A
984
Q

Tidal volume (TV?

A

volume inspired or expired with each breath at rest

500ml in males, 350ml in females

985
Q

Inspiratory reserve volume (IRV)?

A

2-3 L

maximum volume of air that can be inspired at the end of a normal tidal inspiration

inspiratory capacity = TV + IRV

986
Q

Expiratory reserve volume (ERV)?

A

750ml

maximum volume of air that can be expired at the end of a normal tidal expiration

significantly reduced in obesity (increased abdominal fat mass pushes up against the diaphragm, reducing the volume of air that can be expelled)

987
Q

Residual volume (RV)?

A

1.2L

volume of air remaining after maximal expiration
increases with age

RV = FRC - ERV

988
Q

Functional residual capacity (FRC)?

A

the volume in the lungs at the end-expiratory position

FRC = ERV + RV

989
Q

Vital capacity (VC)?

A

5L

maximum volume of air that can be expired after a maximal inspiration

4,500ml in males, 3,500 mls in females

decreases with age

VC = inspiratory capacity + ERV

990
Q

Total lung capacity (TLC)?

A

around 6L (4-6L)

sum of the vital capacity + residual volume

maximal volume of gas in the lungs after a maximal inspiration

991
Q

Physiological dead space (VD) (lung volumes)?

A

VD = tidal volume * (PaCO2 - PeCO2) / PaCO2

where PeCO2 = expired air CO2

992
Q

No Abx prescribing or delayed Abx prescribing is generally recommended for pts with what?

A

acute otitis media, acute sore throat/acute pharyngitis/acute tonsillitis, common cold, acute rhinosinusitis or acute cough/acute bronchitis

993
Q

Immediate Abx prescribing approach may be considered for pts with what?

A

children younger than 2 years with bilateral acute otitis media

children with otorrhoea who have acute otitis media

patients with acute sore throat/acute pharyngitis/acute tonsillitis when 3 or more Centor criteria are present

994
Q

Centor criteria for sore throat?

A

presence of tonsillar exudate
tender anterior cervical lymphadenopathy or lymphadenitis
history of fever
absence of cough

995
Q

If 3+ of the centor criteria are present what does this mean?

A

there is 40-60% chance the sore throat is caused by Group A beta-haemolytic Streptococcus so give Abx

996
Q

If pt is at risk of developing Cx, an immediate Abx prescribing policy is recommended. Examples?

A
  • systemically very unwell
  • S&S suggestive of serious illness and/or complications (particularly pneumonia, mastoiditis, peritonsillar abscess, peritonsillar cellulitis, intraorbital or intracranial complications)
  • pre-existing comorbidity. eg. patients with significant heart, lung, renal, liver or neuromuscular disease, immunosuppression, cystic fibrosis, and young children who were born prematurely
  • > 65 yrs with acute cough and two or more of the following, or older than 80 years with acute cough and one or more of the following:
    hospitalisation in previous year; type 1 or type 2 diabetes; history of congestive heart failure; current use of oral glucocorticoids;
997
Q

Examples of how long resp tract infections may last?

A

acute otitis media: 4 days

acute sore throat/acute pharyngitis/acute tonsillitis: 1 week

common cold: 1 1/2 weeks

acute rhinosinusitis: 2 1/2 weeks

acute cough/acute bronchitis: 3 weeks

998
Q

Differential diagnosis for chronic SOB?

A

heart failure
asthma
aortic stenosis
recurrent PE
lung ca
pulmonary fibrosis
bronchiectasis
anaemia
obesity

999
Q

Aortic stenosis main features?

A

Chest pain, SOB and syncope seen in symptomatic patients
An ejection systolic murmur radiating to the neck and narrow pulse pressure are found on examination

1000
Q

If pt smokes, find out about what?

A
  • smoking behaviour
  • level of nicotine dependence
  • previous quitting attempts
1001
Q

Mx if pt wishes to quit smoking?

A
  • refer to NHS Stop Smoking Services
  • drug Tx to reduce withdrawl= NRT, varenicline or bupropion
    (most effective= vareniciline or combination NRT- patch + short acting preparation)
1002
Q

Review once seen pt wishing to stop smoking?

A

review 2w after stopping smoking (for NRT or 3-4w after with V or B), then CO level measured at 4w

then professional judgement

if taking V then can reduce dose to 500ug 2xd
stop V or B if develop agitation, depressed mood

1003
Q

What to do if pt wants to stop smoking and use e-cigarettes?

A

use stop smoking medicine instead; if still want to then give info and support and referral

1004
Q

What could you offer pts who don’t want to or not ready to stop smoking?

A

harm reduction approach eg:
- stop smoking but continue to use NRT
- cut down before stopping, with or without NRT
- temporary abstinence, with or without NRT
- can use NRT as long as needed to prevent relapse

1005
Q

What type of pts should be strongly encouraged to take up referral to stop smoking services?

A
  • aged 12-17yrs
  • pregnancy women (incl who have stopped in past 2w or CO reading 4ppm+)
  • mothers of young children, esp breastfeeding

if unwilling then risk and benefits of NRT and offer practical advice. Use clinical judgement whether to prescribe NRT to pregnant or young people

1006
Q

Can pregnant/breastfeeding/young pts be prescribed varenicline or bupropion to help stop smoking?

A

NO

1007
Q

How to ask about pts dependence on smoking and nicotine dependence?

A
  • how many cigarretes per day
  • how soon after waking do they smoke their 1st
1008
Q

What level of CO reading in expired air is classed as a non-smoker?

A

10ppm or less

1009
Q

Practical advise to help pt stop smoking?

A
  • set quit date and commit
  • 1st few days hardest and may get withdrawl symptoms but start to improve after 3rd or 4th day
  • craving set off by: stress, seeing others smoke, being intoxicated
  • manage cravings= short bouts of exercise eg. brisk walk; talking to friend; keep busy eg. game on phone or drink glass of water; change environment eg. another room/outside
  • abrupt quitting eg. not a puff rule is most successful
1010
Q

Medical Mx for stopping smoking?

A

NRT, varenicline or bupropion.

Only one not any together

Combination NRT OR varenicline most effective

combination NRT= patch + short acting preparation

depends of pts preference and contraindications

Prescribe 2w of NRT or 3-4w of varenicline or bupropion then only give further prescriptions to pts who have demonstrated their attempt to quitting is continuing

1011
Q

Withdrawl symptoms of smoking cessation?

A

irritability, frustration, anger, anxiety, difficulty concentrating, increased appetitie, restlessness, depressed, insomnia

weight gain eg. 5-9kg but less likely with drug Tx

1012
Q

NRT for smoking cessation?

A

NRT= patch for 16hrs or 24hrs for background cravings and faster acting eg. lozenge or mouth spray for breakthrough urges. Don’t have acidic drinks (coffee/fruit juice) in 15mins before oral NRT. Start NRT on quit date

1013
Q
A
1014
Q
A
1015
Q
A
1016
Q
A
1017
Q
A
1018
Q

Varenicline for smoking cessation?

A
  • start 7-14 days before quit date. (unavailable until further notice)
  • recommended course is 12w (monitor regular and only continue if not smoking)
1019
Q

Bupropion for smoking cessation?

A

start 7-14d before quit date. 150mg prolonged release tablets.

1020
Q

If pt is unsuccessful using NRT, varenicline or bupropion, what should you do?

A

not offer a repeat prescription within 6m unless special circumstances have intervened

1021
Q

Can you combine NRT, varenicline or bupropion?

A

no

1022
Q

When should you offer a combination of NRT for smoking cessation?

A

NRT patches and another form of NRT (gum, inhalator, lozenge or nasal spray) to pts who show high level of dependence on nicotine or have found single forms of NRT inadequate in past

1023
Q

Varenicline (for smoking cessation) MOA?

A

nicotininic receptor partial agonist

1024
Q

Adverse effects of NRT?

A

nausea and vomiting, headaches and flu-like symptoms

1025
Q

Adverse effects of varenicline?

A

nausea (common), headache, insomnia, abnormal dreams

1026
Q

Use varenicline (smoking cessation) in caution in who? Contraindications?

A
  • caution= Hx of depression or self-harm
  • contraindicated= pregnancy and breast feeding
1027
Q

Bupropion (smoking cessation) MOA?

A

norepinephrine and dopamine reuptake inhibitor, and nicotinic antagonist

1028
Q

Bupropion has a small risk of what? Contraindicated in?

A
  • small risk of seizures (1 in 1000)
  • contraindication= epilepsy, pregnancy and breast feeding. Having eating disorder is relative contraindication.
1029
Q

NICE recommended in 2010 that all pregnant women should be tested for smoking using what?

A

CO detectors, partly as some women find difficult to say they smoke due to pressures not to during pregnancy

1030
Q

What pregnant women should be referred to NHS Stop Smoking Services?

A

all that smoke; stopped smoking within last 2w; CO reading of 7ppm or +

1031
Q

Interventions for pregnant women that smoke?

A

1st= CBT, motivational interviewing or structured self-help and support from NHS Stop Smoking Services

  • NRT if above measures fail, remove before bed, no evidence affects childs birthweight
  • varenicline and bupropion contraindicated
1032
Q

Very brief advice for any pt that says they smoke?

A
  • ask current and past smoking behaviour
  • verbal and written info on risks of smoking and benefits of stopping
  • options for quitting= behavioural support, meds, e-cigs
  • refer to stop smoking service if want to
1033
Q

Advice to pt who doesn’t want to stop smoking?

A
  • advise to think about and encourage to return if decide to
  • ask to adopt harm reduction approach
  • record their smoking status & every opportunity ask again in sensitive way
1034
Q

What is transfer factor?

A

describes the rate at whichc a gas will diffuse from alveoli into blood

1035
Q

What is used to test transfer factor (the rate at which a gas will diffuse from alveoli into blood)?

A

carbon monoxide: results may be given as the total gas transfer (TLCO) or that corrected for lung volume (transfer coefficient, KCO)

1036
Q

Causes of a raised TLCO? (transfer factor)

A
  • asthma
  • pulmonary haemorrhage (e.g. granulomatosis with polyangiitis, Goodpasture’s)
  • left-to-right cardiac shunts
  • polycythaemia
  • hyperkinetic states
  • male gender, exercise
1037
Q

Causes of lower TLCO? (transfer factor)

A

pulmonary fibrosis
pneumonia
pulmonary emboli
pulmonary oedema
emphysema
anaemia
low cardiac output

1038
Q

What conditions may cause an increased KCO with a normal or reduced TLCO?

A
  • KCO tends to increase with age

-pneumonectomy/lobectomy

-scoliosis/kyphosis

  • neuromuscular weakness
  • ankylosis of costovertebral joints e.g. ankylosing spondylitis
1039
Q

a

A