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RACP 2024 > Respiratory > Flashcards

Respiratory Flashcards

1
Q

What is the pathophysiology associated with acute pulmonary embolism?

A

Occlusion of pulmonary artery results in ventilated areas without perfusion (V/Q mismatch)
Increased pulmonary vascular resistance results in increased pulmonary artery pressure, increased RV afterload resulting in RV dilatation and dysfunction
RV dysfunction results in reduced LV preload and cardiac output, resulting in RV ischaemia

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2
Q

How should a possible PE be assessed?

A

-Negative Wells criteria + negative PERC excludes PE
-Positive PERC perform D-dimer and use YEARS algorithm
- Positive Wells or raised d-dimer perform CTPA or imaging

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3
Q

Should asymptomatic or subsegmental PE be treated?

A

No, higher risk of 90-day mortality in anti-coagulated group

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4
Q

How long should a PE be treated for?

A

Provoked:
- transient risk factor = 3 months
- permanent risk factor = lifelong

Unprovoked: 3-6 months
- consider prophylactic NOAC

Submassive PE: 6-12 months

Massive PE: indefinite

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5
Q

When is thrombolysis indicated for PE?

A

Massive PE if SBP<90 or falls by 40 or

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6
Q

When is an IVC filter indicated for PE?

A

Patients with contraindication to anticoagulation:
Recent surgery
Haemorrhagic CVA
Active bleeding
Massive PE where recurrent embolism would be fatal
Recurrent PE despite anticoagulation

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7
Q

What follow up is indicated after a PE?

A

Massive PE or ongoing symptoms are 3-6 months: repeat CTPA and ECHO to rule out chronic disease

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8
Q

When should a thrombophilia screen be performed as part of work up for PE?

A

If under 40 and unprovoked PE

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9
Q

What should be included on a thrombophilia screen for PE?

A

Antithrombin 3
Protein C
Protein S
Factor 5 leiden
Plasminogen
Fibrinogen
Activated protein C resistance
Cardiolipin antibody

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10
Q

What is the pathological diagnosis of pneumonia?

A

Acute infection of lung parenchyma resulting in alveolar occlusion with inflammatory infiltrates

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11
Q

What are common pathogens that cause pneumonia?

A

Most common = Strep pneumonia
Others: mycoplasma pneumoniae, Staph aureus, Legionella pneumophilia, enterobacteriaceae, haemophilus influenzae

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12
Q

What therapies for COVID-19 infection have demonstrated a reduction in mortality?

A

Dexamethasone
Tocilizumab/baricitinib

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13
Q

What are the three most common causes of pleural effusions?

A
  1. Malignancy
  2. Heart failure
  3. Infection (including TB)
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14
Q

What medications can cause a pleural effusion?

A

MADCOPIN

Methotrexate
Amiodarone
Dasatinib
Clozapine
Ovarian stimulation
Phenytoin
Immunotherapy
Nitrofurantoin

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15
Q

What is the mode of essential imaging for suspected pleural effusion?

A

Point of care thoracic ultrasound

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16
Q

What is the first step in diagnosis of a new pleural effusion of unclear aetiology?

A

Diagnostic thoracocentesis

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17
Q

What are the contraindications to a diagnostic thoracocentesis?

A
  • insufficient pleural fluid
  • skin infection or wound at the needle insertion site
  • severe bleeding risk
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18
Q

What are the common complications to thoracocentesis? Which is the most common?

A

Most common = pneumothorax

Pain at puncture site
Breathlessness, cough
Bleeding
Empyema
Soft tissue infection
Spleen or liver puncture
Re-expansion pulmonary oedema (rare)

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19
Q

What does “anchovy paste” pleural fluid indicate?

A

Amoebal abscess, can occure with Hepato-pleural fistula

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20
Q

What routine tests should be performed on pleural fluid?

A

Cell count and differential
Total protein (paired with serum)
LDH (paired with serum)
Glucose
Culture and gram stain
Cytology

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21
Q

What is a pleural fluid pH of < 7.2 indicative of?

A

Parapneumonic effusion

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22
Q

What is the difference between a transudate and an exudate?

A

Transudate = imbalance between hydrostatic and oncotic pressure in chest

Exudate = result from inflammation and impaired lymphatic drainage

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23
Q

What are causes for a transudative pleural effusion?

A

Heart failure (may present as exudate after long period of diuresis)
CSF leak
Atelectasis
Hepatic hydrothorax
Hypoalbuminaemia
Hypothyroidism (can also be exudate)
Nephrotic syndrome
Peritoneal dialysis
Urinothorax

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24
Q

What are common causes of exudative effusions?

A

Malignancy
Infection
Autoimmune conditions
Chylothorax
Cholesterol effusion seen in TB, RA
ARDS
Asbestos pleural effusion
Pancreatitis, abdo infection
Hypothyroidism
Radiation therapy
PE

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25
Q

What is Light’s criteria for pleural effusions?

A

Exudate if any one positive:
-Fluid protein : serum protein > 0.5
-Pleural fluid LDH : serum LDH > 0.6
-Pleural LDH >2/3 serum LDH ULN

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26
Q

What is the pleural fluid only three test combination rule?

A

Exudate is defined as any one of:
-Pleural fluid protein > 30
- pleural fluid cholesterol > 55
- Pleural LDH >2/3 serum LDH ULN

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27
Q

What factors influence the management approach of a malignant pleural effusion?

A

Patient preference
Prognosis
Presence of non-expandable lung (means pleurodesis will not be effective)

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28
Q

What is a trapped lung and how is it determined?

A

Inability of lung to expand fully to fill the thoracic cavity usually due to presence of fibrinous restrictive pleural layer

Can be determined by post aspiration CXR

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29
Q

What is the most effective management strategy for malignant pleural effusions?

A

No evidence to support any one strategy being more effective than the other

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30
Q

What are the different management strategies for malignant pleural effusions?

A

-Repeated therapeutic pleural aspirations
-talc slurry pleurodesis via 12Fr intercostal catheter
-talc slurry pleurodesis via Large bore chest drain
- indwelling pleural catheter
- talc pouldrage pleurodesis via thorascopy
- video assisted thoracoscopic pleurodesis

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31
Q

What are the 3 pathophysiological features of asthma?

A

Variable airflow obstruction
Bronchial hyper-responsiveness
Airway inflammation

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32
Q

What reasons may someone with asthma have no bronchodilator reversibility on spirometry?

A

Baseline FEV1 is normal
Recent bronchodilator use
Poorly controlled asthma

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33
Q

What tests can be employed to diagnose asthma?

A

Two week peak flow monitoring at home
Exhaled nitric oxide
Raised blood eosinophilia

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34
Q

What is samter’s triad variant of asthma?

A

Asthma, aspirin intolerance, nasal polyps

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35
Q

What is the allergic bronchopulmonary aspergillosis variant of asthma?

A

Chronic asthma
Recurrent pulmonary infiltrates
Bronchiectasis
Very high total IgE (>1000)
Evidence of aspergillus senstivity

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36
Q

What is the EGPA (eosinophillic granulomatosis with polyangitis, previously Churg-Strauss) variant of asthma?

A

Necrotising vasculitis, granulomas, tissue eosinophilia
Asthma + blood eosinophils essential
30-50% ANCA positive
Cardiac disease accounts for 50% deaths
Often don’t involve kidneys

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37
Q

In what patients with asthma may long term oral steroids be required?

A

Those with adrenal insufficiency
Allergic bronchopulmonary aspergillosis varian
EGPA

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38
Q

What add on therapies can be used and when in severe asthma?

A

-Tiotropium: evidence of airflow obstruction,
exacerbations
- macrolides: exacerbations, cough + sputum
- monteleukast: aspirin sensitive asthma
- mAbs: exacerbations, type 2 biomarkers

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39
Q

What is the biggest risk factor for COPD? What are other risk factors?

A

Smoking - causal in 50% of cases

Air pollution, esp indoor cooking over open flame
Asthma
Infection
Occupational dusts
Low SES

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39
Q

What mABs are available for severe asthma? What are their benefits?

A

Omalizumab: targets IgE, used in allergic asthma
Mepolizumab: targets IL5R in eosinophilic asthma
Benralizumab: targets IL5R in eosinophillic asthma
Dupilumab: targets IL4/IL13R in allergic/eosinophillic asthma with ectopy

Steroid sparing therapies
Reduce exacerbations by 50%

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40
Q

How is COPD diagnosed ?

A

Persistent airflow limitation that is not fully reversible = post bronchodilator FEV1/FVC <0.7 (LLN)

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41
Q

What non-pharmacologic therapies are useful in COPD?

A

Minimise exposures
Pulmonary rehab programme = 2x/week 8 week programme

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42
Q

What pharmacological therapy is used in COPD?

A

SABA or SAMA PRN
THEN add regular LAMA or LABA
THEN combo LAMA/LABA
THEN add ICS

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43
Q

What interventions prevent disease deterioration in COPD?

A

Smoking cessation
Vaccinations: influenza, COVID and pneumococcal

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44
Q

What features define COPD exacerbations and how should they be managed?

A

Increased SOB and/or cough that worsens in < 14 days

70% are caused by infection but need to work up other causes such as cardiac, anaemia, anxiety

Inhaled bronchodilators
PO steroids - short course
PO antibiotics
Oxygen aiming sats 88-92%, NIV
PT and airway clearance
Smoking cessation
Inhaler technique

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45
Q

What is the COPD=X guideline for management of COPD?

A

Confirm diagnosis with spirometry
Optimise function with pulmonary rehab and inhalers
Prevent deterioration with smoking cessation and vaccination
Develop plan of care with self-management action plan
Manage exacerbations

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46
Q

What is bronchiectasis?

A

Permanent dilatation of bronchi and bronchioles due to destruction of airway muscles and elastic connective tissue

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47
Q

What are common causes of bronchiectasis?

A
  • post infection
  • ABPA = allergic bronchopulmonary aspergillosis
  • COPD
  • traction secondary to fibrosis
  • aspiration
  • obstruction
  • immunodeficiencies
  • congenital (Marfans, ciliary defects, A1AT deficiency)
  • Inflammatory (RA, coeliac, DPB, SLE, IBD)
  • Young’s syndrome (Male chronic rhinosinusitis, infertility, bronchiectasis)
  • Amyloidosis
  • cystic fibrosis
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48
Q

What investigations should be used in the work up of bronchiectasis?

A

CT chest
3 sputums for AFBs
IgE, Aspergillus precipitin
Immunoglobulins
Functional assessment

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49
Q

What is the main bacteria that affects people with bronchiectasis? What makes it challenging to treat?

A

Pseudomonas aeruginosa
Forms biofilms (pili)
Intrinsic resistance to beta-lactams

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50
Q

What are non-pseudomonal bacteria that cause exacerbations in bronchiectasis?

A

Non-tuberculous mycobacteria
Aspergillus
Atenotrophomonas maltophilia
Staphylococcus aureus

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51
Q

What antibiotics do you treat acute bronchiectasis exacerbations with?

A

Guided by sputum culture: 10 days PO ABx
If pseudomonas then 14 days ciprofloxacin

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52
Q

How should chronic inflammation in bronchiectasis be managed?

A

Macrolides (erythromycin)
OR
oral steroids

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53
Q

Through what 8 mechanisms do macrolides reduce inflammation in bronchiectasis?

A
  • impair production of pro-inflammatory cytokines such as TNF-a
  • inhibit neutrophil adhesion to cells
  • inhibit respiratory burst of neutrophils
  • reduce mucus secretion from airways
  • improve macrophage clearance of apoptotic cells
  • inhibit quorum sensing signals decreasing pseudomonal biofilm development
  • decrease reflux and microaspiration
  • impair epithelial cell growth and fibroblast migration
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54
Q

What are potential harms of macrolides used to treat bronchiectasis?

A
  • Increased resistance
  • Impairs intracellular killing of mycobacteria in macrophages, possibly increasing NTM infections
  • QTc prolongation (Avoid concurrent ciprofloxacin prescription)
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55
Q

How are chronic infections treated in bronchiectasis?

A

-Inhaled antibiotics such as tobramycin
- trial other PO antibiotics
- macrolide or doxycycline

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56
Q

How are NTM infections treated in bronchiectasis?

A

First need to ensure they are pathogenic

MAC = ERClar = ethambutol + rifampicin + clarithromycin 12 months

M. Abscessus = cefotoxitin + amikacin IV for 1 month then clarithromycin + doxycycline + ciprofloxacin for 12 months

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57
Q

What is the commonest genetically life limiting inherited condition in caucasians?

A

Cystic fibrosis

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58
Q

What is the the pathological basis of cystic fibrosis? What is the inheritance pattern of cystic fibrosis?

A

Defect in CFTR on Chr7 = non-functioning Na/K pump results in dehydration of mucus, reducing mucocilliary clearance, leading to bacterial colonisation and airway inflammation + destruction

Most commonly is class II due to CFTR-trafficking defect = no functional protein

Autosomal recessive

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59
Q

What classification of CFTR protein defect is ivacaftor used in? How does it work?

A

Class III = defective channel regulation (G551D mutations)

CFTR potentiator and allows channel to open

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60
Q

How is CF diagnosed?

A

Clinical presentation usually at birth with meconium ileus

Heel prick test = immunoreactive trypsinogen (high sensitivity, low specificity)
To confirm diagnosis then sweat test with Cl > 60 mmol/L (borderline 40-60)
Gene testing

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61
Q

What therapies are effective for cystic fibrosis?

A
  • CFTR modulators
  • Inhaled DNase
  • macrolides (azithromycin)
  • hypertonic saline
  • Lung transplantation
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62
Q

How do tezacaftor and elexacaftor work?
What patients are they used in?

A

CFTR correctors that move protein to cell surface

Given in combination with ivacaftor for heterozygous DF508 mutations

63
Q

What is the DF508 mutation?

A

Single deletion of amino acid in the CFTR protein

64
Q

What criteria need to be met in order for an adult patient with CF to be referred for lung transplant?

A
  • FEV1 < 35%pred
  • increasing frequency of IVAbs
  • pO2 < 60
  • pCO2 > 50
  • clinical organism resistance
  • impaired QoL
65
Q

What organisms cause chronic infections in CF?

A

Staph aureus
Haemophilus influnzae
Pseudomonas aeruginosa

66
Q

What is the significance of Mycobacterium abscessus with regard to lung transplantation in CF?

A

Active infection is contraindication to transplant

67
Q

How is bone disease managed in CF

A
  • calcium and vitamin D supplements
  • Screen with DEXA every 2 years
  • bisphosphonates
68
Q

How is fertility managed in CF?

A

Women on modulators able to get pregnant, otherwise can use assisted conception

Men born without vas deferens so need assisted conception

Should have genetic counselling/screening

69
Q

What is normal sleep architecture?

A

3-5 cycles of NREM and REM sleep per night

NREM = 80% total sleep time, has 3 stages N1/N2/N3. N3 = deepest most restorative sleep

REM = atonia, tonic/phasic eye movement, 20% total sleep time

70
Q

What is the sleep architecture of narcolepsy?

A

Intrusion of REM into periods of wakefulness

71
Q

What is the sleep architecture of REM behaviour disorder?

A

Intrusion of wakefulness features into REM

72
Q

What are the four types of sleep study? Which is the gold standard?

A

Type 1 = laboratory polysomnography = gold standard. 7 channels.

Type 2 = portable study of 7 channels (at home). Contraindicated in neuromuscular weakness or hypoventilation, intellectual impairment, seizures, parasomnias

Type 3 = 4 channels, used for screening

Type 4 = overnight oximetry + HR, used for screening

73
Q

What is apnoea and hypoapnoea?

A

Apnoea = cessation of airflow for at least 10s

Hypopnoea = reduction in airflow by 30% for at least 10s + 4% O2 desat or EEG arousal

74
Q

What is the apnoea-hypopnoea index (AHI)?

A

Marker of severity of apnoeas and hypopnoeas per hour
Normal < 5/hour
Mild 5-15/hour
Moderate 15-30/hour
Severe >30/hour

75
Q

How is sleep hypoventilation confirmed on polysomnography?

A

Transcutaneous CO2 (TcCO2) >55 for >10 minutes
OR
>10 increase in TcCO2 during sleep to a value > 50

76
Q

What are the characteristics of OSA?

A

upper airway narrowing with ongoing respiratory effort
On sleep study see a cessation of airflow followed by desaturation with ongoing respiratory effort

77
Q

What are the characteristics of CSA?

A

reduction/cessation in airflow due to absent/reduced respiratory effort

On sleep study seen absent airflow followed by desaturation+ absent effort

78
Q

What are the characteristics of sleep hypoventilation?

A

Abnormal increase in PaCO2 with sleep (seen in NM disorders, OHS)

79
Q

What is the diagnostic criteria of OSA?

A

AHI >5/hour + symptoms
OR
AHI >15/hour +/- symptoms

80
Q

What are the sensitivity and specificity of OSA screening tools in general?

A

Highly sensitive
Low specificity

81
Q

What is the Epworth Sleepniess score?

A

Subjective measure of sleepiness
Not sensitive or specific to diagnose OSA
Poor correlation with OSA severity

82
Q

What treatments are available for OSA?

A
  • Risk factor modification: weight loss, reduce alcohol, position, avoid respiratory depressant meds
  • CPAP
  • tonsillectomy
  • bariatric surgery
83
Q

What are the clinical features of obesity hypoventilation syndrome?

A
  1. Awake hypercapnia (PaCO2 > 45)
  2. BMI > 30
  3. Sleep disordered breathing with other causes of hypoventilation included
84
Q

What are treatments for obesity hypoventilation syndrome?

A
  • weight loss
  • positive airway pressure: CPAP if co-existing OSA, NIV if not
85
Q

When is adaptive servo ventilation indicated?

A

For central sleep apnoea in patients with LVEF > 45%

86
Q

What is narcolepsy type 1?

A

Excessive daytime sleepiness for at least 3 months with 1 of:
- definite cataplexy with a positive MSLT
- low CSF hypocretin

87
Q

What is narcolepsy type 2?

A

Excessive daytime sleepiness for at least 3 months with positive MSLT, normal CSH hypocretin without cataplexy

88
Q

What is the pathophysiological basis for narcolepsy?

A

Autoimmune destruction of hypothalamic neurones that produce hypocretin (orexin), which causes arousal and transition between wake and sleep

89
Q

What is cataplexy?

A

Sudden and transient episode of muscle weakness associated with conscious awareness usually triggered by emotions

90
Q

How is narcolepsy treated?

A

Stimulants: dexamphetamine, modafinil, armodafinil
SSRI or SNRI for cataplexy

91
Q

How is narcolepsy diagnosed?

A

PSG followed by Mean Sleep Latency Test
UDS

MSLT <8 minutes associated with 2 sleep onset REM periods is suggestive of narcolepsy

92
Q

What is REM sleep behaviour disorder?

A

Loss of usual muscle atonia during REM - dream re-enactment

Associated with alpha-synucelinopathies; Lewy body dementia, Parkinson’s disease, multiple system atrophy

93
Q

What treatments are available for REM sleep behaviour disorder?

A

Bedroom safety
Melatonin or clonazepam
Screening for neurodegenerative disorder

94
Q

What is the definition of insomnia and what is best management?

A

Difficulties falling asleep, staying asleep or achieving restorative sleep which affects daytime function and quality of life

Best treatment is cognitive behavioural therapy

95
Q

What are the phases of a flow-volume loop?

A

Starts at full inspiration
Forced expiration = peak flow
70% vital capacity expelled in first second of breath = FEV1
Lung volume expelled = FVC
Completed through inhalation back to TLC

96
Q

What is seen on spirometry of obstructive airways disease?

A

Inhomogenous narrowing of airways results in slowed airway emptying during expiration = reduced FEV1 with preserved FVC = scalloping of expiratory loop
PEFR falls with morse severe disease
Inspiratory loop preserved due to traction from intrapleural pressure

97
Q

How is FEV1 z-score used to define obstructive airway disease severity?

A

Mild: -2.5 to -1.65
Moderate: -4 to -2.5
Severe: < -4

98
Q

What is seen on a flow volume loop of restrictive airways disease?

A

Reduction in FVC disproportionate to FEV1 = loop shape preserved but amplitude diminishes

Must be confirmed by measurement of lung volumes

99
Q

How does upper airway obstruction affect spirometry?

A
  • Fixed large airway obstruction (tracheal stenosis) = flattening of expiratory and inspiratory flow loops
  • variable intrathoracic large airway obstruction (tracheal polyp, vocal cord paralysis, non-circumferential tumours) = flattening of expiratory loop but preservation of inspiratory loop
    -variable extrathoracic large airway obstruction = preserved expiratory loop, flattening of inspiratory loop
100
Q

How is an A-a gradient calculated from an ABG? What is it’s significance?

A

A-a = {FIO2 x (Patm - 47) - ((1.25 x (PaCO2))} - PaO2
Where at at sea level + 0.21 FIO2 FIO2 x (Patm - 47) = 150

Normal = (age/4) + 4

A-a gradient measures ability of air transfer from alveoli to artery. Normal A-a indicates hypoventilation, elevated A-a gradient indicates shunt (PE, pneumonia)

101
Q

By what amount does HCO3 increase to compensate for resp acidosis?

A

Acute: HCO3 increases by 1 for every 10 mmHg rise in PaCO2

Chronic: HCO3 increases by 4 for every 10 mmHg rise in PaCO2

102
Q

By what amount does HCO3 decrease to compensate for resp alkalosis?

A

Acute: HCO3 decreases by 2 for every 10 mmHg rise in PaCO2

Chronic: HCO3 decrease by 5 for every 10 mmHg rise in PaCO2

103
Q

What is Winter’s formula for metabolic acidosis?

A

Calculates predicted CO2 compensation for a given HCO3

Expected PaCO2 = (1.5 x HCO3) + 8 +/- 2

If higher than expected then inadequate compensation OR co-existant respiratory acidosis

If lower than expected co-existent respiratory alkalosis

104
Q

How is an anion gap calculated and interpreted?

A

(Na + K) - (Cl + HCO3)

Normal anion gap = (0.2 x Alb) + (1.5 x phosphate) = 4-12

105
Q

What features of HRCT chest suggest pulmonary fibrosis?

A

Reticulation (fine lines in subpleural lung)
Traction bronchiectasis
Honeycombing
Architectural distortion
Volume loss

106
Q

What are the radiological features of the following ILD types:
- usual interstitial pneumonia (UIP)
- Non-specific interstitial pneumonia (NSIP)
- Organising pneumonia (OP)
- Desquamative interstitial pneumonia (DIP)
- Respiratory bronchiolitis interstitial lung disease (RB-ILD)
- lymphocytic interstitial pneumonia (LIP)
- hypersensitivity pneumonitis (HP)

A

UIP: subpleural reticulation, apical basal gradient, traction bronchiectasis, honeycombing

NSIP: ground glass change, apical basal gradient, subpleural sparing, traction bronchiectasis

OP: consolidation, bronchovascular in distribution

DIP: ground glass change with small cysts

RB-ILD: centrilobular ground glass nodularity

LIP: ground glass changes with cysts

HP: acute = ground glass nodularity, chronic = subpleural reticulation, apical basal gradient, traction bronchiectasis, honeycombing, with ground glass and gas trapping (mosaicism)

107
Q

What are the basic management principles of ILD?

A

Avoid exposure +/- immunosuppress:
- pneumoconiosis
- iatrogenic
- hypersensitivty pneumonitis
- histiocytosis
- smoking-related

Observe +/- immunosuppress:
- sarcoidosis
- CTD-ILD, IPAF
- Idiopathic LIP
- COP
- NSIP

108
Q

What type of ILD can anti-fibrotics (pirfenidone/nintedanib) be used in?

A

Idiopathic pulmonary fibrosis
OR
Nintedanib can be used in any progressive fibrosing interstitial lung disease

109
Q

How is IPF diagnosed?

A

Progressive fibrosing condition in which other causes excluded with radiological features of UIP =subpleural reticulation, apical basal gradient, traction bronchiectasis, honeycombing

Needs discussion at ILD-MDM

Rarely need surgical biopsy

110
Q

What risk factors are associated with IPF?

A

Older age (can be familial)
Male
Smoking history
GORD
Family history of ILD

111
Q

How is IPF treated?

A

NOT with immunosuppressants (except steroids in acute exacerbation)

Use anti-fibrotics: pirfenidone, nintedanib

112
Q

What is the mechanism of action, benefit and side effects of Pirfenidone and Nintedanib?

A

Neither have symptom benefit

Pirfenidone:
- Reduced TGF-B and fibroblast proliferation
- slows disease progression (preserves FVC) and improves survival
- SEs: nausea/GI upset, photosensitivity rash (sun protection)

Nintedanib:
- Inhibits multiple tyrosine kinases (PDGF, VEGF, FGF)
- slow disease progression (preserved FVC) and reduces incidence of exacerbations
- SEs: diarrhoea, weight loss, increases CV risk, small bleeding risk

113
Q

What connective tissue disorders are most commonly associated with ILD and what radiological type is seen?

A
  • RA - UIP (subpleural reticulation, apical basal gradient, traction bronchiectasis, honeycombing)
  • Systemic sclerosis - NSIP (ground glass change, apical basal gradient, subpleural sparing, traction bronchiectasis)
  • Idiopathic inflammatory myopathies - OP (consolidation, bronchovascular in distribution)
  • Sjogrens - LIP (ground glass changes with cysts)
114
Q

How can hypersensitivity pneumonitis be differentiated from IPF radiologically?

A

Presence of ground glass and/or gas trapping

115
Q

How is hypersensitivity pneumonitis treated?

A

Avoid exposure +/- immunosuppression +/- nintedanib (if fibrosis present)

116
Q

What are the smoking related ILDs?

A

RB-ILD
DIP
Langerhans cell histiocytosis

117
Q

What are the indications for treatment of sarcoidosis?

A

-Treat life or organ threatening disease
-treat quality of life altering disease

118
Q

What is the most common cause to least common cause of pulmonary hypertension?

A

Most common = Left heart disease
Lung disease
Rare: pulmonary artery hypertension and CTEPH/obstructive and obscure

119
Q

What are the 5 subtypes of pulmonary hypertension?

A

Group 1: isolated precapillary pulmonary hypertension = PAH = CTD, drug induced
Group 2: pulmonary hypertension due to left heart disease
Group 3: pulmonary arterial hypertension due to lung disease and hypoxia (cor pulmonale)
Group 4: pulmonary artery obstruction (CTEPH)
Group 5: obscure mechanisms

120
Q

What investigations are used for pulmonary hypertension?

A

1st: Echocardiogram (peak TR)
Then consider role of V/Q scan (gold standard) and right heart catheter

121
Q

How can right heart catheter distinguish different types of pulmonary hypertension?

A

Pulmonary hypertension = mPAP > 20 mmHg

-PAH: wedge pressure< 15 and PVR>2
-Isolated post capillary(Ipc): wedge pressure > 15 and PVR<2
-combined pre and post capillary (Cpc): wedge pressure > and PVR >2

122
Q

What 3 pathways are targeted in PAH and what treatments target these pathways?

A
  1. Endothelin pathway (endothelin receptor antagonists block vasoconstriction and proliferation):
    - ambriesantan
    - bosentan
    - macitentan
  2. Nitric oxide pathway(PDE5i promote vasodilation and reduce proliferation via cGMP):
    - sildenafil
    - tadalafil
    - Riociguat
  3. Prostacyclin pathway (increase cAMP to promote vasodilation and reduce proliferation):
    - epoprostenol (IV)
    - iloprost (Neb)
    - selexipag (oral)
123
Q

In which types of pulmonary hypertension should vasodilators be used?

A

Group 1 = PAH

Not in group 2 as can precipitate pulmonary oedema
Not in group 3 as disturbs autoregulation and can increase blood flow to unventilated lung causing hypoxaemia

124
Q

What are indications for listing for lung transplantation for cystic fibrosis?

A
  • chronic respiratory failure (type 1 or 2)
  • NIV dependence
  • frequent hospitalisations (infections, haemoptysis)
  • pulmonary hypertension
  • rapid decline
125
Q

What are indications for listing COPD patients for lung transplant?

A
  • bode index >=7
  • very severe airflow obstruction (FEV1 <20%)
  • frequent exacerbations
  • hypercapnic respiratory failure
126
Q

What are indications for listing for lung transplant in ILD?

A
  • 10% decline in FVC over 6/12
  • 15% decline in DLCO over 6/12
  • O2 sats <88% on 6MWT
  • Distance <250m OR decline in distance by 50m over 6/12
  • pulmonary hypertension
  • Worsening CT fiindings
127
Q

How are patients with pulmonary hypertension assessed for lung transplant?

A

Stratified into risk group:
- low risk
- intermediate-low risk
- intermediate-high risk
- high risk

High risk patients have poorer outcomes:
- higher mortality on waitlist
- higher need for urgent transplant
- higher mortality post transplant
- higher risk chronic lung allograft dysfunction

Intermediate risk patients should be listed for transplant

128
Q

What are absolute contraindications to lung transplantation?

A

Recent malignancy:
- could transplant if cancer free survival > 5 years
- could transplant if prostate cancer with low Gleason score

Certain infections:
- Burkholderia cepacia

Untreatable other organ dysfunction (heart, liver, kidney) unless co-transplant

Uncorrectable bleeding diathesis

Significant chest wall or spinal deformity

129
Q

What are relative contraindications to lung transplantation?

A

BMI > 30
Infection with TB, NTM
Lack of rehab efforts
Age >65
Acute medical deterioration
Previous thoracic surgery

130
Q

How are lung transplants matched?

A

Blood group
Size
Presence of preformed antibodies

131
Q

What are complications of lung transplant?

A

Early:
- bleeding
- primary graft dysfunction
- pleural and other surgical complications
- AKI
(donor mismatch no longer occurs)

Intermediate:
- acute cellular rejection
- acute antibody mediated rejection
- airway complications (dehiscence, stenosis)
- Vascular (pulmonary vein stenosis)
- PE
- infection
- metabolic (phosphate)

Late:
- chronic lung allograft dysfunction
- post transplant lymphoproliferative disorder
- malignancy (skin)
- primary disease recurrence
- hypertension
- renal impairment (calcineurin inhibitor toxicity)
- post transplant diabetes

132
Q

What proportion of lung transplant recipients develop bronchiolitis obliterans 5 years post transplant?

133
Q

What is the leading cause of cancer death?

A

Lung cancer

134
Q

What is the most common subtype of lung cancer?

A

Non-small cell lung cancer (NSCLC), specifically adenocarcinoma

135
Q

What is the recommendation for lung cancer screening (is not currently in practice)?

A

CT scan 1-2 years for those aged 50-70 who smoked 30+ pack years and who currently smoke or quit smoking in the past 10 years

Reduces mortality from lung cancer

136
Q

What is the underlying principle of a liquid biopsy for lung cancer?

A

Performing a blood or urine test and diagnosing cancer based on the presence of circulating tumour DNA (ctDNA), microRNA or circulating tumour cells (CTCs)

137
Q

What treatment modalities can be used for curative intent in Stage 1 or 2 NSCLC?

A

Stage 1:
- Surgical resection
- Stereotactic radiotherapy

Stage 2:
- Stereotactic radiotherapy +/- chemotherapy

138
Q

What is the treatment for locally advanced NSCLC (T3 orT4, or those with Nodal disease)?

A

Most not surgical candidates

Chemoradiotherapy followed by immunotherapy is curative intent in most cases

If has EGFR, ALK or ROS1 mutations can have TKI (first line for IIIB stage disease)

139
Q

What is the treatment of metastatic NSCLC?

A

Most are palliative intent
- TKIs for EGFR, ALK and ROS1 mutations
- chemoimmunotherapy
- immunotherapy
- chemotherapy followed by immunotherapy
- best supportive care
- palliative radiotherapy to mets

140
Q

What frequency are EGFR, ALK and ROS1 mutations found in NSCLCs?

A
  • EGFR: 10-30%, 60% Asians
  • ALK: 5% (gene rearrangements)
  • ROS1: 1-2%
141
Q

What are some EGFR TKIs used in NSCLC?

A

Gefitinib
Erlotinib
Afatinib
Osimertinib

142
Q

What are some ALK TKIs used in NSCLC?

A

Crizotinib
Ceritinib
Alectinib
Brigatinib
Lorlatinib

143
Q

What are some ROS1 TKIs used in NSCLC?

A

Crizotinib
Entrectinib

144
Q

What are immunotherapies used in NSCLC?

A

Anti-PD1:
- pembrolizumab (single agent or with chemo)
- nivolumab (2nd line after platinum doublet chemo OR with ipilimumab for stage IV)

Anti-PDL1:
- Atezolizumab: (in combo with platinum doublet chemo + bevacizumab, 2nd line after progression on chemo, or in SCLC)
- durvalumab: unresectable stage III after platinum based chemo

145
Q

What proportion of SCLC present with metastatic disease?

146
Q

What imaging features suggest a diagnosis of SCLC?

A
  • bulky thoracic lymph node involvement
  • Mets to contralateral lung, brain, liver, adrenals, bones
147
Q

What paraneoplastic syndromes is SCLC associated with?

A
  • SIADH
  • Cushing syndrome
  • Lambert-eaton syndrome
  • encephalomyelitis
  • sensory neuropathy syndromes
  • dermatomyositis
  • hyperglycaemia
  • hypoglycaemia
  • hypercalcaemia
  • gynecomastia
148
Q

Is there a role for CT screening of SCLC?

A

No, does not detect at earlier stage and does not improve survival

149
Q

How is metastatic SCLC managed?

A

Chemotherapy (cisplatin-etoposide) +/- immunotherapy +/- chest radiotherapy

150
Q

What subtype of mesothelioma carries the best prognosis?

A

Epithelioid

151
Q

What is the management of mesothelioma?

A

All palliative intent

Manage pain and breathlessness (meds or radiotherapy)
Manage pleural fluid (drainage, IPC, talc pleurodesis)
Cisplatin or carboplatin + pemetrexed chemo
Immunotherapy (Nivo + ipi, or Ipi alone)

152
Q

What mechanical ventilation strategies should be used for ARDs?

A
  • low tidal volumes and inspiratory pressures
  • prone positioning
  • high frequency oscillatory ventilation
  • Higher PEEP
153
Q

What are indications for NIV?

A

Hypercapnic respiratory failure, less effective for type 1 resp failure
- acute exacerbations of COPD
- cardiogenic pulmonary oedema
- obesity and obesity hypoventilation
- weaning from invasive ventilation
- post extubation failure
- chest wall disease and neuromuscular disease
- palliative care and do not intubate
- bridge to transplant
- very old patients with community acquired pneumonia

154
Q

Is there a role of epworth sleepiness score in neuromuscular disease?

155
Q

What ventilator setting should be used in ARDS?

A
  • low tidal volumes and inspiratory pressures (6mL/kg)
  • prone positioning
156
Q

What factors may indicate NIV failure?

A
  • severe acidosis (pH < 7.25)
  • marked de novo hypoxaemia (PaO2/FiO2 < 200)
  • respiratory distress
  • non pulmonary organ failure

RACP 2024 (15 decks)

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