Respiratory Flashcards
1
Q
Should asymptomatic or subsegmental PE be treated?
A
No, higher risk of 90-day mortality in anti-coagulated group
2
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
3
Q
When is thrombolysis indicated for PE?
A
Massive PE if SBP<90 or falls by 40 or
4
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
5
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
6
Q
When should a thrombophilia screen be performed as part of work up for PE?
A
If under 40 and unprovoked PE
7
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
8
Q
What are common pathogens that cause pneumonia?
A
Most common = Strep pneumonia
Others: mycoplasma pneumoniae, Staph aureus, Legionella pneumophilia, enterobacteriaceae, haemophilus influenzae
9
Q
What are the three most common causes of pleural effusions?
A
- Malignancy
- Heart failure
- Infection (including TB)
10
Q
What medications can cause a pleural effusion?
A
MADCOPIN
Methotrexate
Amiodarone
Dasatinib
Clozapine
Ovarian stimulation
Phenytoin
Immunotherapy
Nitrofurantoin
11
Q
What is the mode of essential imaging for suspected pleural effusion?
A
Point of care thoracic ultrasound
12
Q
What is the first step in diagnosis of a new pleural effusion of unclear aetiology?
A
Diagnostic thoracocentesis
13
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
14
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)
15
Q
What does “anchovy paste” pleural fluid indicate?
A
Amoebal abscess, can occure with Hepato-pleural fistula
16
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
17
Q
What is a pleural fluid pH of < 7.2 indicative of?
A
Parapneumonic effusion
18
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
19
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
20
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
21
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
22
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
23
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)
24
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
25
What is the most effective management strategy for malignant pleural effusions?
No evidence to support any one strategy being more effective than the other
26
What are the different management strategies for malignant pleural effusions?
-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
27
What reasons may someone with asthma have no bronchodilator reversibility on spirometry?
Baseline FEV1 is normal
Recent bronchodilator use
Poorly controlled asthma
28
What tests can be employed to diagnose asthma?
Two week peak flow monitoring at home
Exhaled nitric oxide
Raised blood eosinophilia
29
What is samter's triad variant of asthma?
Asthma, aspirin intolerance, nasal polyps
30
What is the allergic bronchopulmonary aspergillosis variant of asthma?
Chronic asthma
Recurrent pulmonary infiltrates
Bronchiectasis
Very high total IgE (>1000)
Evidence of aspergillus senstivity
31
What is the EGPA (eosinophillic granulomatosis with polyangitis, previously Churg-Strauss) variant of asthma?
Necrotising vasculitis, granulomas, tissue eosinophilia
Asthma + blood eosinophils essential
30-50% ANCA positive
Cardiac disease accounts for 50% deaths
Often don't involve kidneys
32
In what patients with asthma may long term oral steroids be required?
Those with adrenal insufficiency
Allergic bronchopulmonary aspergillosis varian
EGPA
33
What add on therapies can be used and when in severe asthma?
-Tiotropium: evidence of airflow obstruction,
exacerbations
- macrolides: exacerbations, cough + sputum
- monteleukast: aspirin sensitive asthma
- mAbs: exacerbations, type 2 biomarkers
34
What is the biggest risk factor for COPD? What are other risk factors?
Smoking - causal in 50% of cases
Air pollution, esp indoor cooking over open flame
Asthma
Infection
Occupational dusts
Low SES
34
What mABs are available for severe asthma? What are their benefits?
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%
35
How is COPD diagnosed ?
Persistent airflow limitation that is not fully reversible = post bronchodilator FEV1/FVC <0.7 (LLN)
36
What non-pharmacologic therapies are useful in COPD?
Minimise exposures
Pulmonary rehab programme = 2x/week 8 week programme
37
What pharmacological therapy is used in COPD?
SABA or SAMA PRN
THEN add regular LAMA or LABA
THEN combo LAMA/LABA
THEN add ICS
38
What interventions prevent disease deterioration in COPD?
Smoking cessation
Vaccinations: influenza, COVID and pneumococcal
39
What features define COPD exacerbations and how should they be managed?
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
40
What is the COPD=X guideline for management of COPD?
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
41
What is bronchiectasis?
Permanent dilatation of bronchi and bronchioles due to destruction of airway muscles and elastic connective tissue
42
What are common causes of bronchiectasis?
- 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
43
What investigations should be used in the work up of bronchiectasis?
CT chest
3 sputums for AFBs
IgE, Aspergillus precipitin
Immunoglobulins
Functional assessment
44
What is the main bacteria that affects people with bronchiectasis? What makes it challenging to treat?
Pseudomonas aeruginosa
Forms biofilms (pili)
Intrinsic resistance to beta-lactams
45
What are non-pseudomonal bacteria that cause exacerbations in bronchiectasis?
Non-tuberculous mycobacteria
Aspergillus
Atenotrophomonas maltophilia
Staphylococcus aureus
46
What antibiotics do you treat acute bronchiectasis exacerbations with?
Guided by sputum culture: 10 days PO ABx
If pseudomonas then 14 days ciprofloxacin
47
How should chronic inflammation in bronchiectasis be managed?
Macrolides (erythromycin)
OR
oral steroids
48
What are potential harms of macrolides used to treat bronchiectasis?
- Increased resistance
- Impairs intracellular killing of mycobacteria in macrophages, possibly increasing NTM infections
- QTc prolongation (Avoid concurrent ciprofloxacin prescription)
49
How are chronic infections treated in bronchiectasis?
-Inhaled antibiotics such as tobramycin
- trial other PO antibiotics
- macrolide or doxycycline
50
How are NTM infections treated in bronchiectasis?
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
51
How is CF diagnosed?
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
52
What therapies are effective for cystic fibrosis?
- CFTR modulators
- Inhaled DNase
- macrolides (azithromycin)
- hypertonic saline
- Lung transplantation
53
What criteria need to be met in order for an adult patient with CF to be referred for lung transplant?
- FEV1 < 35%pred
- increasing frequency of IVAbs
- pO2 < 60
- pCO2 > 50
- clinical organism resistance
- impaired QoL
54
What organisms cause chronic infections in CF?
Staph aureus
Haemophilus influnzae
Pseudomonas aeruginosa
55
What is the significance of Mycobacterium abscessus with regard to lung transplantation in CF?
Active infection is contraindication to transplant
56
How is bone disease managed in CF
- calcium and vitamin D supplements
- Screen with DEXA every 2 years
- bisphosphonates
57
How is fertility managed in CF?
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
58
What is normal sleep architecture?
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
59
What is the sleep architecture of narcolepsy?
Intrusion of REM into periods of wakefulness
60
What is the sleep architecture of REM behaviour disorder?
Intrusion of wakefulness features into REM
61
What are the four types of sleep study? Which is the gold standard?
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
62
What is the diagnostic criteria of OSA?
AHI >5/hour + symptoms
OR
AHI >15/hour +/- symptoms
63
What are the sensitivity and specificity of OSA screening tools in general?
Highly sensitive
Low specificity
64
What is the Epworth Sleepniess score?
Subjective measure of sleepiness
Not sensitive or specific to diagnose OSA
Poor correlation with OSA severity
65
What treatments are available for OSA?
- Risk factor modification: weight loss, reduce alcohol, position, avoid respiratory depressant meds
- CPAP
- tonsillectomy
- bariatric surgery
66
What are the clinical features of obesity hypoventilation syndrome?
1. Awake hypercapnia (PaCO2 > 45)
2. BMI > 30
3. Sleep disordered breathing with other causes of hypoventilation included
67
What are treatments for obesity hypoventilation syndrome?
- weight loss
- positive airway pressure: CPAP if co-existing OSA, NIV if not
68
What treatments are available for REM sleep behaviour disorder?
Bedroom safety
Melatonin or clonazepam
Screening for neurodegenerative disorder
69
What is the definition of insomnia and what is best management?
Difficulties falling asleep, staying asleep or achieving restorative sleep which affects daytime function and quality of life
Best treatment is cognitive behavioural therapy
70
What is seen on spirometry of obstructive airways disease?
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
71
How is FEV1 z-score used to define obstructive airway disease severity?
Mild: -2.5 to -1.65
Moderate: -4 to -2.5
Severe: < -4
72
What is seen on a flow volume loop of restrictive airways disease?
Reduction in FVC disproportionate to FEV1 = loop shape preserved but amplitude diminishes
Must be confirmed by measurement of lung volumes
73
How does upper airway obstruction affect spirometry?
- 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
74
What features of HRCT chest suggest pulmonary fibrosis?
Reticulation (fine lines in subpleural lung)
Traction bronchiectasis
Honeycombing
Architectural distortion
Volume loss
75
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)
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)
76
What are the basic management principles of ILD?
Avoid exposure +/- immunosuppress:
- pneumoconiosis
- iatrogenic
- hypersensitivty pneumonitis
- histiocytosis
- smoking-related
Observe +/- immunosuppress:
- sarcoidosis
- CTD-ILD, IPAF
- Idiopathic LIP
- COP
- NSIP
77
What type of ILD can anti-fibrotics (pirfenidone/nintedanib) be used in?
Idiopathic pulmonary fibrosis
OR
Nintedanib can be used in any progressive fibrosing interstitial lung disease
78
How is IPF diagnosed?
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
79
What risk factors are associated with IPF?
Older age (can be familial)
Male
Smoking history
GORD
Family history of ILD
80
How is IPF treated?
NOT with immunosuppressants (except steroids in acute exacerbation)
Use anti-fibrotics: pirfenidone, nintedanib
81
What is the mechanism of action, benefit and side effects of Pirfenidone and Nintedanib?
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
82
What connective tissue disorders are most commonly associated with ILD and what radiological type is seen?
- 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)
83
How can hypersensitivity pneumonitis be differentiated from IPF radiologically?
Presence of ground glass and/or gas trapping
84
How is hypersensitivity pneumonitis treated?
Avoid exposure +/- immunosuppression +/- nintedanib (if fibrosis present)
85
What are the smoking related ILDs?
RB-ILD
DIP
Langerhans cell histiocytosis
86
What are the indications for treatment of sarcoidosis?
-Treat life or organ threatening disease
-treat quality of life altering disease
87
What is the most common cause to least common cause of pulmonary hypertension?
Most common = Left heart disease
Lung disease
Rare: pulmonary artery hypertension and CTEPH/obstructive and obscure
88
What are the 5 subtypes of pulmonary hypertension?
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
89
What investigations are used for pulmonary hypertension?
1st: Echocardiogram (peak TR)
Then consider role of V/Q scan (gold standard) and right heart catheter
90
How can right heart catheter distinguish different types of pulmonary hypertension?
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
91
What 3 pathways are targeted in PAH and what treatments target these pathways?
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)
92
In which types of pulmonary hypertension should vasodilators be used?
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
93
What are indications for listing for lung transplantation for cystic fibrosis?
- chronic respiratory failure (type 1 or 2)
- NIV dependence
- frequent hospitalisations (infections, haemoptysis)
- pulmonary hypertension
- rapid decline
94
What are indications for listing COPD patients for lung transplant?
- bode index >=7
- very severe airflow obstruction (FEV1 <20%)
- frequent exacerbations
- hypercapnic respiratory failure
95
What are indications for listing for lung transplant in ILD?
- 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
96
How are patients with pulmonary hypertension assessed for lung transplant?
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
97
What are absolute contraindications to lung transplantation?
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
98
What are relative contraindications to lung transplantation?
BMI > 30
Infection with TB, NTM
Lack of rehab efforts
Age >65
Acute medical deterioration
Previous thoracic surgery
99
How are lung transplants matched?
Blood group
Size
Presence of preformed antibodies
100
What are complications of lung transplant?
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
101
What proportion of lung transplant recipients develop bronchiolitis obliterans 5 years post transplant?
50%
102
What is the leading cause of cancer death?
Lung cancer
103
What is the most common subtype of lung cancer?
Non-small cell lung cancer (NSCLC), specifically adenocarcinoma
104
What is the recommendation for lung cancer screening (is not currently in practice)?
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
105
What is the underlying principle of a liquid biopsy for lung cancer?
Performing a blood or urine test and diagnosing cancer based on the presence of circulating tumour DNA (ctDNA), microRNA or circulating tumour cells (CTCs)
106
What treatment modalities can be used for curative intent in Stage 1 or 2 NSCLC?
Stage 1:
- Surgical resection
- Stereotactic radiotherapy
Stage 2:
- Stereotactic radiotherapy +/- chemotherapy
107
What is the treatment for locally advanced NSCLC (T3 orT4, or those with Nodal disease)?
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)
108
What is the treatment of metastatic NSCLC?
Most are palliative intent
- TKIs for EGFR, ALK and ROS1 mutations
- chemoimmunotherapy
- immunotherapy
- chemotherapy followed by immunotherapy
- best supportive care
- palliative radiotherapy to mets
109
What frequency are EGFR, ALK and ROS1 mutations found in NSCLCs?
- EGFR: 10-30%, 60% Asians
- ALK: 5% (gene rearrangements)
- ROS1: 1-2%
110
What are some EGFR TKIs used in NSCLC?
Gefitinib
Erlotinib
Afatinib
Osimertinib
111
What are some ALK TKIs used in NSCLC?
Crizotinib
Ceritinib
Alectinib
Brigatinib
Lorlatinib
112
What are some ROS1 TKIs used in NSCLC?
Crizotinib
Entrectinib
113
What are immunotherapies used in NSCLC?
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
114
What proportion of SCLC present with metastatic disease?
2/3rds
115
What imaging features suggest a diagnosis of SCLC?
- bulky thoracic lymph node involvement
- Mets to contralateral lung, brain, liver, adrenals, bones
116
What paraneoplastic syndromes is SCLC associated with?
- SIADH
- Cushing syndrome
- Lambert-eaton syndrome
- encephalomyelitis
- sensory neuropathy syndromes
- dermatomyositis
- hyperglycaemia
- hypoglycaemia
- hypercalcaemia
- gynecomastia
117
Is there a role for CT screening of SCLC?
No, does not detect at earlier stage and does not improve survival
118
How is metastatic SCLC managed?
Chemotherapy (cisplatin-etoposide) +/- immunotherapy +/- chest radiotherapy
119
What subtype of mesothelioma carries the best prognosis?
Epithelioid
120
What is the management of mesothelioma?
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)
121
What mechanical ventilation strategies should be used for ARDs?
- low tidal volumes and inspiratory pressures
- prone positioning
- high frequency oscillatory ventilation
- Higher PEEP
122
What are indications for NIV?
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
123
Is there a role of epworth sleepiness score in neuromuscular disease?
No
