General Flashcards

1
Q

What are the features of moderate asthma exacerbation?

A

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

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2
Q

What are the features of severe asthma exacerbation

A

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

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3
Q

What are the features of a lifetheatening asthma attack?

A

PEFR < 33% best or predicted
Oxygen sats < 92%
‘Normal’ pC02 (4.6-6.0 kPa)
Silent chest, cyanosis or feeble respiratory effort
Bradycardia, dysrhythmia or hypotension
Exhaustion, confusion or coma

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4
Q

What does a normal pCO2 mean in an acute asthma attack?

A

Exhausation
Treat as life threatening

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5
Q

How many features in the life threatening section need to be present to treat as a life threatening asthma attack?

A

Any one

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6
Q

Management of acute asthma exacerbation?

A

Oxygen
Bronchodilation - SABA
Corticosteroid
- 40/50mg predinoslone for 5 days
Ipratroium
IV magnesium sulphate
IV aminophylline

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7
Q

What is the criteria for discharge in asthma attack?

A

Stable on discharge medication - no nebs or O2 for 12 hours
PEF > 75 % of predicted

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8
Q

Most common organisms causing infective exacerbation of COPD?

A

Haemophilus influenzae
Streptococcus pneumiae
Moraxella

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9
Q

Antibitoic choice in infective exacerbation of COPD?

A

Amoxicllin
Clrithromycin
Doxycycline

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10
Q

Causes of acute respiratory distress syndrome?

A

infection: sepsis, pneumonia
massive blood transfusion
trauma
smoke inhalation
acute pancreatitis
Covid-19
cardio-pulmonary bypass

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11
Q

Criteria for Acute respiratory distress syndrome?

A

acute onset (within 1 week of a known risk factor)
pulmonary oedema: bilateral infiltrates on chest x-ray (‘not fully explained by effusions, lobar/lung collapse or nodules)
non-cardiogenic (pulmonary artery wedge pressure needed if doubt)
pO2/FiO2 < 40kPa (300 mmHg)

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12
Q

What are the featues of allergic boronchopulmonary aspergillosis?

A

bronchoconstriction: wheeze, cough, dyspnoea. Patients may have a previous label of asthma
bronchiectasis (proximal)

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13
Q

Investigations 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

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14
Q

Bronchiectasis + eosinphillia?

A

Allergic bronchopulmonary aspergillosis

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15
Q

What are the genetics behind alpha-1 antitrypsin deficiency?

A

Chromosome 14
Autosomal recessive / co-dominant fashion

Normal genotype: PiMM

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16
Q

In alpha 1 antitrypsin how does PiMZ present?

A

carrier and unlikely to develop emphysema if a non-smoker

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17
Q

In alpha 1 antitrypsin how does PiSS present?

A

50% A1AT levels
Empysema

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18
Q

Investigations for A1AT?

A

A1AT concentrations
Spiromtetry: Obstructive

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19
Q

What is the spirometry picture in A1AT deficiency?

A

Obstructive

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20
Q

Management of A1AT deficiency?

A

no smoking
supportive: bronchodilators, physiotherapy
intravenous alpha1-antitrypsin protein concentrates
surgery: lung volume reduction surgery, lung transplantation

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21
Q

How can acute mountain sickness (AMS) be treated?

A

Acetazolimide
- it causes a primary metabolic acidosis and compensatory respiratory alkalosis which increases respiratory rate and improves oxygenation

Gain altitude by no more than 500 meters per day

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22
Q

How to interpret arterial blood gas?

A
  1. How is the patient?
  2. Is the patient hypoxaemic?
    the Pa02 on air should be >10 kPa
  3. Is the patient acidaemic (pH <7.35) or alkalaemic (pH >7.45)
  4. Respiratory component: What has happened to the PaCO2?
    PaCO2 > 6.0 kPa suggests a respiratory acidosis (or respiratory compensation for a metabolic alkalosis)
    PaCO2 < 4.7 kPa suggests a respiratory alkalosis (or respiratory compensation for a metabolic acidosis)
  5. Metabolic component: What is the bicarbonate level/base excess?
    bicarbonate < 22 mmol/l (or a base excess < - 2mmol/l) suggests a metabolic acidosis (or renal compensation for a respiratory alkalosis)
    bicarbonate > 26 mmol/l (or a base excess > + 2mmol/l) suggests a metabolic alkalosis (or renal compensation for a respiratory acidosis)
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23
Q

What does Respiratory = opposite mean?

A

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

ROME

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24
Q

What does metabolic = equal mean?

A

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

ROME

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25
Q

Types of asbestosis lung disease?

A

Pleural plaques
Pleural thickening
Asbestosis
Mesothelioma
Lung cancer

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26
Q

How are pleural plaques from asbestosis managed?

A

Benign
Do not require follow up

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27
Q

What lobe does asbestosis typically affect?

A

Lower lobe fibrosis

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28
Q

Features of asbestosis ?

A

dyspnoea and reduced exercise tolerance
clubbing
bilateral end-inspiratory crackles
lung function tests show a restrictive pattern with reduced gas transfer

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29
Q

What is the most dangerous type of asbestos ?

A

Crocodile blue

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30
Q

Features of mesothelioma?

A

progressive shortness-of-breath
chest pain
pleural effusion

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31
Q

What is the prognosis of mesothelioma?

A

8-14 months

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32
Q

What is the most common cancer from asbestosis?

A

Lung cancer

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33
Q

What type of cancer is mesothelioma?

A

Malignant disease of the pleura

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34
Q

What test is now done to test for asthma as a diagnosis?

A

fractional exhaled nitric oxide (FeNO)

Looks for inducible nitric oxide from eosinophils

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35
Q

How is asthma diagnosed in > 17 year olds?

A
  1. Better off from work –> specialist referral for occupational asthma
  2. FeNO on everyone
  3. Spironometry + bronchodilator reversibility testing
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36
Q

How is asthma diagnosed in children?

A
  1. Spirometry
  2. If spirometry is normal or, obstructive + no bronchodilator reversibility –> FeNO test
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37
Q

What is considered a diagnostic level for FeNO in adults?

A

in adults level of >= 40 parts per billion (ppb) is considered positive

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38
Q

What is considered a diagnostic level for FeNO in children?

A

in children level of >= 35 parts per billion (ppb) is considered positive

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39
Q

What is considered an obstructive picture on FEV1 to FVC

A

70% or less is considered diagnostic

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40
Q

What is considered a positive reversibility test in adults?

A

n improvement in FEV1 of 12% or more and increase in volume of 200 ml or more

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41
Q

Management of asthma?

A
  1. SABA
  2. SABA + Low dose ICS
  3. SABA + low-dose ICS + leukotriene receptor antagonist (LTRA)
  4. SABA + low-dose ICS + long-acting beta agonist (LABA), (LTRA depending on response)
  5. SABA +/- LTRA - Switch ICS/LABA for a maintenance and reliever therapy (MART), that includes a low-dose ICS
  6. SABA +/- LTRA + medium-dose ICS MART
  7. SABA +/- LTRA + one of the following options:
    - increase ICS to high-dose (only as part of a fixed-dose regime, not as a MART)
    - a trial of an additional drug (for example, a long-acting muscarinic receptor antagonist or theophylline)
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42
Q

What is Maintenance and reliever therapy (MART) for asthma?

A

combined ICS and LABA treatment

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43
Q

What is a low dose ICS?

A

< 400 micrograms

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44
Q

What is a medium dose ICS?

A

400-800 micrograms

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45
Q

What is a high dose ICS?

A

> 800 micrograms

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46
Q

Causes of occupational asthma?

A

isocyanates - the most common cause
example occupations include spray painting and foam moulding using adhesives
platinum salts
soldering flux resin
glutaraldehyde
flour
epoxy resins
proteolytic enzymes

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47
Q

What is atelectasis?

A

postoperative complication in which basal alveolar collapse can lead to respiratory difficulty

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48
Q

Most common causes of bilateral pleural effusion

A

Sarcoidosis
Tuberculosis

Other causes:
lymphoma/other malignancy
pneumoconiosis e.g. berylliosis
fungi e.g. histoplasmosis, coccidioidomycosis

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49
Q

Causes of bronchiectasis?

A

post-infective: tuberculosis, measles, pertussis, pneumonia
cystic fibrosis
bronchial obstruction e.g. lung cancer/foreign body
immune deficiency: selective IgA, hypogammaglobulinaemia
allergic bronchopulmonary aspergillosis (ABPA)
ciliary dyskinetic syndromes: Kartagener’s syndrome, Young’s syndrome
yellow nail syndrome

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50
Q

Management of bronchiectasis?

A
  1. Physical training
  2. Antibiotics for exacerbations + long term rotating antibiotics
  3. Bronchodilator
  4. Immunisation
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51
Q

Most common organisms for exacerbation in bronchiectasis?

A

Haemophilus influenzae (most common)
Pseudomonas aeruginosa
Klebsiella spp.
Streptococcus pneumoniae

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52
Q

Causes of bronchiolitis?

A

RSV (most common)
other causes: mycoplasma, adenoviruses
may be secondary bacterial infection
more serious if bronchopulmonary dysplasia (e.g. Premature), congenital heart disease or cystic fibrosis

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53
Q

Features of bronchiolitis?

A

coryzal symptoms (including mild fever) precede:
dry cough
increasing breathlessness
wheezing, fine inspiratory crackles (not always present)
feeding difficulties associated with increasing dyspnoea are often the reason for hospital admission

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54
Q

Red flags with bronchiolitis?

A

apnoea (observed or reported)
child looks seriously unwell to a healthcare professional
severe respiratory distress, for example grunting, marked chest recession, or a respiratory rate of over 70 breaths/minute
central cyanosis
persistent oxygen saturation of less than 92% when breathing air.

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55
Q

Management of bronchiolitis?

A

coryzal symptoms (including mild fever) precede:
dry cough
increasing breathlessness
wheezing, fine inspiratory crackles (not always present)
feeding difficulties associated with increasing dyspnoea are often the reason for hospital admission

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56
Q

Indications for chest drain insertion?

A

Pleural effusion
Pneumothorax not suitable for conservative management or aspiration
Empyema
Haemothorax
Haemopneumothorax
Chylothorax
In some cases of penetrating chest wall injury in ventilated patients

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57
Q

Insertion of chest drain contraindications?

A

INR > 1.3
Platelet count < 75
Pulmonary bullae
Pleural adhesions

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58
Q

Where should a intercostal chest drain be inserted?

A

5th intercostal space in the midaxillary line

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59
Q

Causes of cavitating lung lesions?

A

abscess (Staph aureus, Klebsiella and Pseudomonas)
squamous cell lung cancer
tuberculosis
Wegener’s granulomatosis
pulmonary embolism
rheumatoid arthritis
aspergillosis, histoplasmosis, coccidioidomycosis

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60
Q

Causes of lung metastasis?

A

breast cancer
colorectal cancer
renal cell cancer
bladder cancer
prostate cancer

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61
Q

Causes of COPD?

A

Smoking
Alpha-1 antitrypsin deficiency

Then the C’s:
cadmium (used in smelting)
coal
cotton
cement
grain

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62
Q

Investigations for COPD?

A

post-bronchodilator spirometry to demonstrate airflow obstruction: FEV1/FVC ratio less than 70%
chest x-ray: hyperinflation, bullae, flat hemidiaphragm. Also important to exclude lung cancer
full blood count: exclude secondary polycythaemia
body mass index (BMI) calculation

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63
Q

Who should be considered for LTOT?

A

very severe airflow obstruction (FEV1 < 30% predicted). Assessment should be ‘considered’ for patients with severe airflow obstruction (FEV1 30-49% predicted)
cyanosis
polycythaemia
peripheral oedema
raised jugular venous pressure
oxygen saturations less than or equal to 92% on room air

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64
Q

How is a patient assessed for LTOT?

A

2 occasions at least 3 weeks apart in patients with stable COPD on optimal management.

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65
Q

Who should be offered LTOT?

A

pO2 of < 7.3 kPa

or
those with a pO2 of 7.3 - 8 kPa with:
- secondary polycythaemia
- peripheral oedema
- pulmonary hypertension

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66
Q

General management of COPD?

A

> smoking cessation advice
replacement therapy, varenicline or bupropion
annual influenza vaccination
one-off pneumococcal vaccination
pulmonary rehabilitation

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67
Q

Management COPD?

A
  1. a short-acting beta2-agonist (SABA) or short-acting muscarinic antagonist (SAMA) is first-line treatment

If this does not work:
2. Assess for asthmatic/steroid responsive features:
- higher blood eosinophil count
- recommend a full blood count for all patients as part of the work-up
- substantial variation in FEV1 over time (at least 400 ml)
- substantial diurnal variation in peak expiratory flow (at least 20%)

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68
Q

Management of COPD with non-asthmatic features?

A
  1. a short-acting beta2-agonist (SABA) or short-acting muscarinic antagonist (SAMA) is first-line treatment
  2. add a long-acting beta2-agonist (LABA) + long-acting muscarinic antagonist (LAMA)

if already taking a SAMA, discontinue and switch to a SABA

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69
Q

Management of COPD with asthmatic features?

A
  1. a short-acting beta2-agonist (SABA) or short-acting muscarinic antagonist (SAMA) is first-line treatment
  2. LABA + inhaled corticosteroid (ICS)

if patients remain breathless or have exacerbations offer triple therapy i.e. LAMA + LABA + ICS
if already taking a SAMA, discontinue and switch to a SABA

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70
Q

When should theophyllinebe considered?

A

recommends theophylline after trials of short and long-acting bronchodilators or to people who cannot used inhaled therapy

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71
Q

Who should be considered for prophylactic antibiotics in COPD?

A

patients should not smoke, have optimised standard treatments and continue to have exacerbations

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72
Q

Choice of prophylactic antibiotics in COPD?

A

Azithromycin

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73
Q

What should be checked before starting azithromycin?

A

ECG to exclude QT prolongation should also be done as azithromycin can prolong the QT interval

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74
Q

Features of cor pulmonale?

A

peripheral oedema, raised jugular venous pressure, systolic parasternal heave, loud P2

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75
Q

What is cryptogenic organising pneumonia?

A

Unknown aetiology
Affects distal bronchioles, respiratory bronchioles, alveolar ducts and alveolar walls

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76
Q

How does cryptogenic organising pneumonia present? Investigations?

A

cough, shortness of breath, fever and malaise.

Invx: Bloods show a leukocytosis and an elevated ESR and CRP
LFT’s may be restrictive, cholecystatic or normal

Imaging typically shows bilateral patchy or diffuse consolidative or ground glass opacities

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77
Q

How does cryptogenic organising pneumonia present? Investigations?

A

cough, shortness of breath, fever and malaise.

Invx: Bloods show a leukocytosis and an elevated ESR and CRP
LFT’s may be restrictive, cholecystatic or normal

Imaging typically shows bilateral patchy or diffuse consolidative or ground glass opacities

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78
Q

Genetics of cystic fibrosis?

A

Cystic fibrosis (CF) is an autosomal recessive disorder
defect in the cystic fibrosis transmembrane conductance regulator gene (CFTR), which codes a cAMP-regulated chloride channel

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79
Q

Where is the mutation in in CF?

A

Most common is delta F508 on the long arm of chromosome 7.

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80
Q

Organisms typically associated with infection in CF?

A

Staphylococcus aureus
Pseudomonas aeruginosa
Burkholderia cepacia*
Aspergillus

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81
Q

Features in cystic fibrosis?

A

neonatal period (around 20%): meconium ileus, less commonly prolonged jaundice
recurrent chest infections (40%)
malabsorption (30%): steatorrhoea, failure to thrive
other features (10%): liver disease

short stature
diabetes mellitus
delayed puberty
rectal prolapse (due to bulky stools)
nasal polyps
male infertility, female subfertility

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82
Q

Management of cystic fiborsis?

A
  1. PT twice daily
  2. Lung transplant - chronic infection with Burkholderia cepacia is an important CF-specific contraindication to lung transplantation

CF should try to minimise contact with each other to prevent cross infection with Burkholderia cepacia complex and Pseudomonas aeruginosa

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83
Q

How to treat homozygous CF?

A

Lumacaftor/Ivacaftor (Orkambi)
-increases the number of CFTR proteins that are transported to the cell surface

ivacaftor is a potentiator of CFTR that is already at the cell surface

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84
Q

What is a contra-indication to lung transplant?

A

chronic infection with Burkholderia cepacia is an important CF-specific contraindication to lung transplantation

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85
Q

Mechanism of salbutamol?

A
  • Short-acting inhaled bronchodilator. Relaxes bronchial smooth muscle through effects on beta 2 receptors
  • Used in asthma and chronic obstructive pulmonary disease (COPD).
  • Salmeterol has similar effects but is long-acting
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86
Q

Mechanism of ipratropium?

A
  • Short-acting inhaled bronchodilator. Relaxes bronchial smooth muscle
  • Used primarily in COPD
  • Tiotropium has similar effects but is long-acting
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87
Q

What drug class is theophylline and what is its mechanism?

A

Methylxanthines
Non-specific inhibitor of phosphodiesterase resulting in an increase in cAMP

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88
Q

What is the new name of churg Strauss syndrome?

A

Eosinophilic granulomatosis with polyangiitis

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89
Q

What are the features of eosinophilic granulomatosis ?

A

asthma
blood eosinophilia (e.g. > 10%)
paranasal sinusitis
mononeuritis multiplex
pANCA positive in 60%

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90
Q

Differences between eosinophilic granulomatosis and granulomatosis with polyangitis?

A
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91
Q

what is idiopathic pulmonary fibrosis?

A

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

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92
Q

What are the features of idiopathic pulmonary fibrosis?

A

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

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93
Q

Features of investigations of idiopathic pulmonary fibrosis?

A

spirometry: classically a restrictive picture (FEV1 normal/decreased, FVC decreased, FEV1/FVC increased)

impaired gas exchange: reduced transfer factor (TLCO)

imaging: bilateral interstitial shadowing (

94
Q

What are the classical imaging findings of idiopathic pulmonary fibrosis?

A

Typically small, irregular, peripheral opacities - ‘ground-glass’ - later progressing to ‘honeycombing’)

95
Q

What is the imaging of choice in idiopathic pulmonary fibrosis?

A

High resolution CT

96
Q

What are the features of kartagener’s syndrome?

A

Dextocardia

dextrocardia or complete situs inversus
bronchiectasis
recurrent sinusitis
subfertility (secondary to diminished sperm motility and defective ciliary action in the fallopian tubes)

97
Q

What is the gram stain of klebsiella?

A

Gram negative rod

98
Q

Features of klebsiella pneumonia?

A

more common in alcoholic and diabetics
may occur following aspiration
‘red-currant jelly’ sputum
often affects upper lobes

99
Q

Mechanism of leyukotrine receptor antagonists?

A

anti-inflammatory and bronchodilatory properties

100
Q

What is Lofgan’s syndrome?

A

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

101
Q

What is the most common pathophysiology of lung abscess?

A

most commonly forms secondary to aspiration pneumonia
poor dental hygiene, previous stroke and reduced consciousness are some of the risk factors for this

102
Q

What are the features of lung carcinoid ?

A

typical age = 40-50 years
smoking not risk factor
slow growing: e.g. long history of cough, recurrent haemoptysis
often centrally located and not seen on CXR
‘cherry red ball’ often seen on bronchoscopy
carcinoid syndrome itself is rare (associated with liver metastases)

103
Q

What are contraindications to surgery in non-small cell lung cancer?

A

assess general health
stage IIIb or IV (i.e. metastases present)
FEV1 < 1.5 litres is considered a general cut-off point*
malignant pleural effusion
tumour near hilum
vocal cord paralysis
SVC obstruction

104
Q

What are the paraneoplastic effects associated with small cell lung cancer?

A

ADH
ACTH - not typical, hypertension, hyperglycaemia, hypokalaemia, alkalosis and muscle weakness are more common than buffalo hump etc
Lambert-Eaton syndrome

105
Q

What are the paraneoplastic effects associated with squamous cell carcinoma?

A

parathyroid hormone-related protein (PTH-rp) secretion causing hypercalcaemia
clubbing
hypertrophic pulmonary osteoarthropathy (HPOA)
hyperthyroidism due to ectopic TSH

106
Q

What are the paraneoplastic effects of adenocarcinoma?

A

gynaecomastia
hypertrophic pulmonary osteoarthropathy (HPOA)

107
Q

Features of small cell lung cancer?

A

usually central
arise from APUD* cells
associated with ectopic ADH, ACTH secretion
ADH → hyponatraemia
ACTH → Cushing’s syndrome
ACTH secretion can cause bilateral adrenal hyperplasia, the high levels of cortisol can lead to hypokalaemic alkalosis
Lambert-Eaton syndrome: antibodies to voltage gated calcium channels causing myasthenic like syndrome

108
Q

What type of cells does small cell lung cancer arise from?

A

APD

Amine - high amine content
Precursor Uptake - high uptake of amine precursors
Decarboxylase - high content of the enzyme decarboxylase

109
Q

Fibrosis affecting the upper lobes?

A

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

110
Q

Fibrosis affecting the lower lobes?

A

idiopathic pulmonary fibrosis
most connective tissue disorders (except ankylosing spondylitis) e.g. SLE
drug-induced: amiodarone, bleomycin, methotrexate
asbestosis

111
Q

Features of Microscopic polyangiitis?

A

renal impairment: raised creatinine, haematuria, proteinuria
fever
other systemic symptoms: lethargy, myalgia, weight loss
rash: palpable purpura
cough, dyspnoea, haemoptysis
mononeuritis multiplex

112
Q

What are the auto-antibodies associated in microscopic polyangitis?

A

pANCA (against MPO) - positive in 50-75%
cANCA (against PR3) - positive in 40%

113
Q

What causes Middle East respiratory syndrome?

A

betacoronavirus MERS-CoV.

114
Q

Contact with what animal causes Middle East respiratory syndrome?

A

Camels

115
Q

Indications for non-invasive ventilation?

A
  • COPD with respiratory acidosis pH 7.25-7.35
  • type II respiratory failure secondary to chest wall deformity, neuromuscular disease or obstructive sleep apnoea
  • cardiogenic pulmonary oedema unresponsive to CPAP
  • weaning from tracheal intubation
116
Q

Pressure for bi-level pressure support in COPD?

A

Expiratory Positive Airway Pressure (EPAP): 4-5 cm H2O
Inspiratory Positive Airway Pressure (IPAP): RCP advocate 10 cm H20 whilst BTS suggest 12-15 cm H2O
back up rate: 15 breaths/min
back up inspiration:expiration ratio: 1:3

117
Q

What are the predisposing factors of obstructive sleep apnea?

A

obesity
macroglossia: acromegaly, hypothyroidism, amyloidosis
large tonsils
Marfan’s syndrome

118
Q

Features of obstructive sleep apnoea?

A

daytime somnolence
compensated respiratory acidosis
hypertension

119
Q

How is sleep apnoea investigated?

A

Epworth Sleepiness Scale - questionnaire completed by patient +/- partner
Best test: polysomography - evaluate abnormalities of sleep by monitoring and quantifying the biophysiological changes
Multiple Sleep Latency Test (MSLT) - measures the time to fall asleep in a dark room during day - follows Polysomnography (using EEG criteria)

120
Q

Management of obstructive sleep apnoea?

A

CPAP

121
Q

Mechanism of omalizumab?

A

IgE mediated asthma

122
Q

Adverse effects of omalizumab?

A

abdominal pain
headache
fever
Churg-Strauss syndrome: may present with eosinophilia, vasculitic rash, worsening respiratory symptoms and peripheral neuropathy

123
Q

Who should be commenced on omalizumab?

A

severe persistent confirmed allergic IgE-mediated asthma
Add on top of standard therapy
oral corticosteroids (defined as 4 or more courses in the previous year)

124
Q

Oxygen dissociation curve shifts to the left?

A

HbF, methaemoglobin, carboxyhaemoglobin
Low [H+] (alkali)
Low pCO2
Low 2,3-DPG
Low temperature

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

125
Q

Oxygen dissociation curve shifts to the right?

A

Raised [H+] (acidic)
Raised pCO2
Raised 2,3-DPG*
Raised temperature

126
Q

What is the L rule for oxygen dislocation ?

A

The L rule

Shifts to L → Lower oxygen delivery, caused by
Low [H+] (alkali)
Low pCO2
Low 2,3-DPG
Low temperature

127
Q

What is the Venturi percentage in a blue Venturi?

A

24% - 2L
Blue

128
Q

What is the Venturi percentage in a white Venturi?

A

28% - 4L
White

129
Q

What is the Venturi percentage in a orange venturi?

A

31% - 6L
Orange

130
Q

What is the Venturi percentage in a yellow venturi?

A

35% - 8L
Yellow

131
Q

What is the Venturi percentage in a red venturi?

A

40% - 10L
Red

132
Q

What is the Venturi percentage in a green venturi?

A

60% - 15L
Green

133
Q

Causes of a transudate pleural effusion <30 ?

A

heart failure (most common transudate cause)
hypoalbuminaemia (liver disease, nephrotic syndrome, malabsorption)
hypothyroidism
Meigs’ syndrome

134
Q

Causes of a transudate pleural effusion >30 ?

A

infection: pneumonia (most common exudate cause), TB, subphrenic abscess
connective tissue disease: RA, SLE
neoplasia: lung cancer, mesothelioma, metastases
pancreatitis
pulmonary embolism
Dressler’s syndrome
yellow nail syndrome

135
Q

What are the parameters for exudate and transudate

A

exudates have a protein level of >30 g/L
transudates have a protein level of <30 g/L

If a pleural effusion has a protein level of 25-30 then lights criteria should be used/

136
Q

What is lights criteria?

A

For protein levels 25-30 in pleural effusion

An exudate is likely if at least one of the following criteria are met:
pleural fluid protein divided by serum protein >0.5
pleural fluid LDH divided by serum LDH >0.6
pleural fluid LDH more than two-thirds the upper limits of normal serum LDH

137
Q

What factors may suggest if a pleural effusion is infected?

A

pH < 7.2
Prulent

*Chest drain should be sited

138
Q

What is the management of recurrent pleural effusions?

A

recurrent aspiration
pleurodesis
indwelling pleural catheter
drug management to alleviate symptoms e.g. opioids to relieve dyspnoea

139
Q

What are features of the CURB65 score?

A

C Confusion (abbreviated mental test score <= 8/10)
Urea >7
R Respiration rate >= 30/min
B Blood pressure: systolic <= 90 mmHg and/or diastolic <= 60 mmHg
65 Aged >= 65 years

0 Low risk
1-2 intermediate risk
3-4 high risk

140
Q

How should CAP be treated?

A

Low risk: Amoxicillin
Higher severity: Amoxicillin + Macrolide

141
Q

What causes psittacosis?

A

Chlamydia psittaci
Obligate intracellular bacteria

142
Q

Features of psittacosis?

A

Signs:
Chest: unilateral crepitations and vesicular breathing (common), evidence of pleural effusion (uncommon)
Abdomen: hepatomegaly and splenomegaly (rare)

Investigations:
Raised inflammatory markers
Chest X-ray: consolidation (90%)
Confirmation with serology (usually as part of atypical pneumonia screening)

143
Q

Management of psittacosis?

A

Treatment:
1st-line: tetracyclines e.g. doxycycline
2nd-line: macrolides e.g. erythromycin

144
Q

Causes of pulmonary eosinophilia?

A

Churg-Strauss syndrome
allergic bronchopulmonary aspergillosis (ABPA)
Loffler’s syndrome
eosinophilic pneumonia
hypereosinophilic syndrome
tropical pulmonary eosinophilia
drugs: nitrofurantoin, sulphonamides
less common: Wegener’s granulomatosis

145
Q

What is loeffler syndrome?

A

Loffler’s syndrome
transient CXR shadowing and blood eosinophilia
thought to be due to parasites such as Ascaris lumbricoides causing an alveolar reaction
presents with a fever, cough and night sweats which often last for less than 2 weeks.
generally a self-limiting disease

146
Q

Features of pulmonary function testing in obstructive lung disease?

A

FEV1 - significantly reduced
FVC - reduced or normal
FEV1% (FEV1/FVC) - reduced

147
Q

Features of pulmonary function testing in restrictive lung disease?

A

FEV1 - reduced
FVC - significantly reduced
FEV1% (FEV1/FVC) - normal or increased

148
Q

Causes of obstructive lung disease?

A

Asthma
COPD
Bronchiectasis
Bronchiolitis obliterans

149
Q

Causes 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

150
Q

What is the pulmonary pressure in pulmonary arterial pressure that classifies as pulmonary hypertension

A

25 mmHg

151
Q

What are the causes of respiratory 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

152
Q

What are the causes of respiratory alkalosis?

A

anxiety leading to hyperventilation
pulmonary embolism
salicylate poisoning*
CNS disorders: stroke, subarachnoid haemorrhage, encephalitis
altitude
pregnancy

153
Q

What is the value of tidal volume?

A

volume inspired or expired with each breath at rest
500ml in males, 350ml in females

154
Q

What is the inspiratory reserve volume?

A

Inspiratory reserve volume (IRV) = 2-3 L
maximum volume of air that can be inspired at the end of a normal tidal inspiration
inspiratory capacity = TV + IRV

155
Q

What is the expiratory reserve volume?

A

Expiratory reserve volume (ERV) = 750ml
maximum volume of air that can be expired at the end of a normal tidal expiration

156
Q

What is the residual volume?

A

Residual volume (RV) = 1.2L
volume of air remaining after maximal expiration
increases with age
RV = FRC - ERV

157
Q

What is the functional residual capacity?

A

Functional residual capacity (FRC)
the volume in the lungs at the end-expiratory position
FRC = ERV + RV

158
Q

What is the vital capacity?

A

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

159
Q

Respiratory problems associated with rheumatoid arthritis?

A

pulmonary fibrosis
pleural effusion
pulmonary nodules
bronchiolitis obliterans
complications of drug therapy e.g. methotrexate pneumonitis
pleurisy
Caplan’s syndrome - massive fibrotic nodules with occupational coal dust exposure
infection (possibly atypical) secondary to immunosuppression

160
Q

Features of sarcoidosis?

A

Non-caseating granulomas

acute: erythema nodosum, bilateral hilar lymphadenopathy, swinging fever, polyarthralgia
insidious: dyspnoea, non-productive cough, malaise, weight loss
skin: lupus pernio
hypercalcaemia: macrophages inside the granulomas cause an increased conversion of vitamin D to its active form (1,25-dihydroxycholecalciferol)

161
Q

Investigation findings in sarcoidosis?

A

A chest x-ray may show the following changes:
stage 0 = normal
stage 1 = bilateral hilar lymphadenopathy (BHL)
stage 2 = BHL + interstitial infiltrates
stage 3 = diffuse interstitial infiltrates only
stage 4 = diffuse fibrosis

Serum ACE

spirometry: may show a restrictive defect
tissue biopsy: non-caseating granulomas
gallium-67 scan - not used routinely

162
Q

What is the management sarcoidosis?

A
  1. Indications for steroids
    patients with chest x-ray stage 2 or 3 disease who are symptomatic. Patients with asymptomatic and stable stage 2 or 3 disease who have only mildly abnormal lung function do not require treatment
    hypercalcaemia
    eye, heart or neuro involvemen
163
Q

Poor Prognostic features of sarcoidosis?

A

insidious onset, symptoms > 6 months
absence of erythema nodosum
extrapulmonary manifestations: e.g. lupus pernio, splenomegaly
CXR: stage III-IV features
black people

164
Q

What is the function of transfer factor?

A

describes the rate at which a gas will diffuse from alveoli into blood. Carbon monoxide is used to test the rate of diffusion

165
Q

What causes a raised total gas transfer (TLCO)

A

asthma
pulmonary haemorrhage (Wegener’s, Goodpasture’s)
left-to-right cardiac shunts
polycythaemia
hyperkinetic states
male gender, exercise

166
Q

What causes a lower total gal transfer?

A

pulmonary fibrosis - asbestosis and others
pneumonia
pulmonary emboli
pulmonary oedema
emphysema
anaemia
low cardiac output

167
Q

HLA DR1 ?

A

Bronchiectasis

168
Q

HLA DR 2 ?

A

SLE

169
Q

HLA DR3 ?

A

autoimmune hepatitis
primary Sjogren syndrome
type 1 diabetes Mellitus
SLE

170
Q

HLA DR 4

A

Rheumatoid

171
Q

HLA DR 27

A

HLA-B27: ankylosing spondylitis, postgonococcal arthritis, acute anterior uveitis

172
Q

Mechanism of bupropion

A

Norepinephrine and dopamine re-uptake inhibitor

173
Q

Primary pneumothorax management?

A

if the rim of air is < 2cm and the patient is not short of breath then discharge should be considered
otherwise,

aspiration should be attempted
if this fails (defined as > 2 cm or still short of breath) then a chest drain should be inserted

174
Q

Management for secondary pneumothorax?

A

if the patient is > 50 years old and the rim of air is > 2cm and/or the patient is short of breath then a chest drain should be inserted.

aspiration should be attempted if the rim of air is between 1-2cm.
f aspiration fails (i.e. pneumothorax is still greater then 1cm) a chest drain should be inserted.

175
Q

If you have had a pneumothorax, what can you not do?

A

scuba diving

176
Q

Cause of farmer’s lung?

A

Saccharopolyspora rectivirgula causes farmer’s lung, a type of EAA

177
Q

What type of hypersensitivity is extrinsic allergic alveoli’s?

A

Acute phase: Type 3
Then delayed past Type 4

178
Q

Examples of extrinsic allergic alveoli’s?

A

bird fanciers’ lung: avian proteins from bird droppings
farmers lung: spores of Saccharopolyspora rectivirgula from wet hay (formerly Micropolyspora faeni)
malt workers’ lung: Aspergillus clavatus
mushroom workers’ lung: thermophilic actinomycetes*

179
Q

Imaging findings for extrinsic allergic alveolitis?

A

Upper zone fibrosis

180
Q

Bronchoalveolar lavage for EAA?

A

Lymphocytosis

181
Q

Is there an eosinohpillia with EAA?

A

No

182
Q

Management of EAA?

A

Steroids

183
Q

COPD: Still breathless and on SAMA / SABA treatment and history of asthma type features?

A

LABA + ICS
Fometerol + ICS

184
Q

Spirometry diagnosis of COPD?

A

Post bronchodilator spirometry FEV1/FVC < 70% of predicted + symptoms of COPD

chest x-ray: hyperinflation, bullae, flat hemidiaphragm. Also important to exclude lung cancer
full blood count: exclude secondary polycythaemia
body mass index (BMI) calculation

185
Q

Causes of bihilar lymphadenopathy?

A

TB
Sarcoid
Fungi: Histoplasmosis coccidioidomycosis
Pneumococcis: Berylliosis
Lymphoma

186
Q

What is used to classify the severity of COPD?

A

FEV1

187
Q

What is normal transfer factor for men and women?

A

80-120

188
Q

Metabolic alkalsois - what respiratory things must be excluded?

A

PE

189
Q

Features of high altitude pulmonary oedema?

A

HAPE presents with classical pulmonary oedema features
Pink frothy cough
Crackles

190
Q

Management of high altitude pulmonary oedema?

A

nifedipine, dexamethasone, acetazolamide, phosphodiesterase type V inhibitors*
oxygen if available
Decent

191
Q

Features of high altitude cerebral oedema?

A

headache, ataxia, papilloedema

192
Q

Very early stage small cell lung carcinoma management?

A

consideration for surgical removal

193
Q

Cannon ball metastasis?

A

Renal cancer - most common

Prostate
Chondrosarcoma

194
Q

Lung mets associated with calcification ?

A

Note - lung mets don’t normally have calcification

195
Q

COPD: Still breathless and on SAMA / SABA treatment and no history of asthma type features?

A

LABA + LAMA

196
Q

Management of allergic bronchopulmonary aspergillosis?

A

Oral glucocorticoids

197
Q

What is alpha 1 antitrypsin?

A

Protase inhibitor for neutrophil elastase

198
Q

What are isocyanates implicated in?

A

Occupational asthma

199
Q

What is friedlander’s pneumonia?

A

Klebsiella pneumonia (Friedlander’s pneumonia) typically occurs in middle-aged alcoholic men
Mortality 30-50%

200
Q

What improve survival in COPD?

A
  1. Smoking cessation
  2. LTOT
201
Q

Spirometry restrictive pattern?

A

Reduced FEV1 (<80% of the predicted normal)
Reduced FVC (<80% of the predicted normal)
FEV1/FVC ratio normal (>0.7)

202
Q

Spirometry obstructive pattern?

A

Reduced FEV1 (<80% of the predicted normal)
Reduced FVC (but to a lesser extent than FEV1)
FEV1/FVC ratio reduced (<0.7)

203
Q

Causes of respiratory 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

204
Q

How does sarcoid increase calcium?

A

increased activity of 1α hydroxylase produced by the sarcoid macrophages.

205
Q

Most common imaging findings in idiopathic pulmonary fibrosis ?

A

Reticular changes worse at bases

IPF - typically affects bases

206
Q

What blood gas should you expect for opiod overdose ?

A

Respiratory acidosis

207
Q

What blood gas should you expect for respiratory alkalosis?

A

anxiety leading to hyperventilation
pulmonary embolism
salicylate poisoning*
CNS disorders: stroke, subarachnoid haemorrhage, encephalitis
altitude
pregnancy

208
Q

WHat blood gas does a salicilate poisoning give and why?

A

Salicylate overdose leads to 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

209
Q

In pleural effusion, what is the criteria for placing a chest tube?

A
  1. If it is turbid or cloud
  2. Presence of organism on gram stain
  3. pH < 7.2
210
Q

Staging of COPD?

A

Post-bronchodilator FEV1/FVC FEV1 (of predicted) Severity
< 0.7 > 80% Stage 1 - Mild - symptoms should be present to diagnose COPD in these patients
< 0.7 50-79% Stage 2 - Moderate
< 0.7 30-49% Stage 3 - Severe
< 0.7 < 30% Stage 4 - Very severe

211
Q

Site of cheset drain insertion?

A

The triangle of safety for chest drain insertion involves the base of the axilla, lateral edge pectoralis major, 5th intercostal space and the anterior border of latissimus dorsi

212
Q

What is bupuprion contraindicated in?

A

Epilepsy

213
Q

What type of drug is varenicline?

A

a nicotinic receptor partial agonist

214
Q

When should varniciline be used with caution?

A

Depression / self harm

215
Q

Smoking cessation in pregnancy?

A

CBT
Varenicline and bupuprion are contradinicated

216
Q

After pneumothorax how long until you can fly?

A

Cannot fly for ideally 1 week, ideally 6

217
Q

Carrier rate of CF?

A

1:25

218
Q

Chlamydia pitasci treatment?

A

Doxycycline

219
Q

What is a catamenial pneumothorax?

A

Catamenial pneumothorax is the cause of 3-6% of spontaneous pneumothoraces occurring in menstruating women

220
Q

How do pleural plaques appear on imaging ?

A

calcified plaques

221
Q

Test to investigate location of airway obstruction

A

Flow volume loop

222
Q

When to assess for LTOT?

A

pO2 of < 7.3 kPa or to those with a pO2 of 7.3 - 8 kPa and one of the following:
secondary polycythaemia
peripheral oedema
pulmonary hypertension

223
Q

What is heerfordt syndrome?

A

subset of sarcoidosis: a combination of parotid enlargement, fever, and anterior uveitis.

224
Q

Test for occupational asthma?

A

Serial peak flow measurements at work and at home are used to detect occupational asthma

225
Q

Causes of sarcoidosis?

A

post-infective: tuberculosis, measles, pertussis, pneumonia
cystic fibrosis
bronchial obstruction e.g. lung cancer/foreign body
immune deficiency: selective IgA, hypogammaglobulinaemia
allergic bronchopulmonary aspergillosis (ABPA)
ciliary dyskinetic syndromes: Kartagener’s syndrome, Young’s syndrome
yellow nail syndrome

226
Q

Surgery to help with alpha 1 antitrypsin?

A

Lung volume reduction

227
Q

CXR findings of allergic bronchopulmonary aspergillosis?

A

Chest x-ray: parenchymal infiltrates with tram track opacities and ring shadows.

228
Q

Most important management in non-CF bronchiectasis?

A

Postural drainage + Inspiratory muscle training

229
Q

Target saturation for COPD until blood gas available?

A

88-92%

230
Q

Recurrent chest infections + subfertility

A

Kartenagers

231
Q

Diet for CF?

A

High calorie + High fat + pancreatic supplement every meal

232
Q

Image findings for silicosis?

A

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