MRCP2 Flashcards
Features of moderate asthma ?
PEFR 50-75% best or predicted
Speech normal
RR < 25 / min
Pulse < 110 bpm
Features of severe asthma?
PEFR 33 - 50% best or predicted
Can’t complete sentences
RR > 25/min
Pulse > 110 bpm
Features of life threatening asthma?
PEFR < 33% best or predicted
Oxygen sats < 92%
Silent chest, cyanosis or feeble respiratory effort
Bradycardia, dysrhythmia or hypotension
Exhaustion, confusion or coma
What is the difference in near fatal asthma?
Elevated CO2
When should you admit a person with severe asthma exacerbation?
When fail to respond to initial therapy
Treatment in life threatening / severe asthma?
- SABA
- Corticosteroid 40-50 mg prednioslone
- Ipratropium bromide
- IV magnesium
- Aminophyline with senior staff consultation
Treatment in life threatening / severe asthma?
- SABA
- Corticosteroid 40-50 mg prednioslone
- Ipratropium bromide
- IV magnesium
- Aminophyline with senior staff consultation
Criteria for discharge in asthma?
been stable on their discharge medication (i.e. no nebulisers or oxygen) for 12–24 hours
inhaler technique checked and recorded
PEF >75% of best or predicted
Most common bacteria for COPD exacerbation?
Haemophilus influenzae (most common cause)
Streptococcus pneumoniae
Moraxella catarrhalis
account for around 30% of exacerbations
Most common viral exacerbation of COPD?
Rhinovirus
On acute review what should you aim saturations at in COPD
prior to the availability of blood gases, use a 28% Venturi mask at 4 l/min and aim for an oxygen saturation of 88-92% for patients with risk factors for hypercapnia but no prior history of respiratory acidosis
adjust target range to 94-98% if the pCO2 is normal
Management of severe COPD?
Nebulised bronchodilator
beta adrenergic agonist: e.g. salbutamol
muscarinic antagonists: e.g. ipratropium
Steroid therapy as above
IV hydrocortisone may sometimes be considered instead of oral prednisolone
IV theophylline
may be considered for patients not responding to nebulised bronchodilators
Indications for NIV?
typically used for COPD with respiratory acidosis pH 7.25-7.35
the BTS guidelines state that NIV can be used in patients who are more acidotic (i.e. pH < 7.25) but that a greater degree of monitoring is required (e.g. HDU) and a lower threshold for intubation and ventilation should be used
bilevel positive airway pressure (BiPaP) is typically used with initial settings:
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
Causes of acute respiratory distress syndrome?
infection: sepsis, pneumonia
massive blood transfusion
trauma
smoke inhalation
acute pancreatitis
Covid-19
cardio-pulmonary bypass
Criteria for acute respiratory distress syndrome?
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)
Aetiology of allergic bronchopulmonary aspergillosis?
Allergy to aspergillis spores
Features of allergic bronchopulmonary aspergillosis?
bronchoconstriction: wheeze, cough, dyspnoea. Patients may have a previous label of asthma
PROXIMAL BRONCHIECTASAIS
Investigation findings of allergic bronchopulmonary aspergillosis?
eosinophilia
flitting CXR changes
positive radioallergosorbent (RAST) test to Aspergillus
positive IgG precipitins (not as positive as in aspergilloma)
raised IgE
Management of allergic bronchopulmonary aaspergillosis ?
- Steroids
- Itraconazole
Pathphysiology of alpha 1 antitrypsin disease ?
Lack of A1AT, lack of protease inhibitor - in non-smokers
Located on chromosome 14
Inherited by a autosomal co-dominant fashion
What is A1AT electrophoresis?
M - for normal
S - for slow
Z - very slow
What is the phenotypes of PiMZ?
if non-smoker low risk of developing emphsema but may pass on A1AT gene to children
What is the phenotype of PiSS?
50% normal levels A1AT
What is the phenotype of PiZZ?
10% normal level
These patients usually manifest disease
lungs: panacinar emphysema, most marked in lower lobes
liver: cirrhosis and hepatocellular carcinoma in adults, cholestasis in children
What are the investigation findings of A1At deficiency?
OBSTRUCTIVE PICTURE
Low A1At levels
Management of A1AT?
no smoking
supportive: bronchodilators, physiotherapy
intravenous alpha1-antitrypsin protein concentrates
surgery: lung volume reduction surgery, lung transplantation
What are the three altitude sicknesses?
Develop 2500 - 3000
Within 6-12 hours :
Acute mountain sickness
High altitude pulmonary oedema
High altitude cerebral oedema
Over 4000 meters - develope:
high altitude pulmonary oedema (HAPE) or high altitude cerebral oedema (HACE),
HACE presents with headache, ataxia, papilloedema
Management of acute mountain sickness?
Correlates to being more physically fit
Gain altitude at no more than 500 m per day
Acetazolamide (a carbonic anhydrase inhibitor) is widely used to prevent AMS and has a supporting evidence base
- it causes a primary metabolic acidosis and compensatory respiratory alkalosis which
- increases respiratory rate and improves oxygenation
How does acetazolamide prevent Acute mountain sickness?
Acetazolamide (a carbonic anhydrase inhibitor) is widely used to prevent AMS and has a supporting evidence base
- it causes a primary metabolic acidosis and compensatory respiratory alkalosis which
- increases respiratory rate and improves oxygenation
What is HACE?
High altitude cerebral oedema
HACE presents with headache, ataxia, papilloedema
Management of HACE?
descent
dexamethasone
Management of HAPE?
descent
nifedipine, dexamethasone, acetazolamide, phosphodiesterase type V inhibitors*
oxygen if available
How should aminophyline be given in COPD and asthma?
For patients not already treated with xanthines (theophylline or aminophylline) a loading dose is given:
dose: 5mg/kg
given by slow intravenous injection over at least 20 minutes
maintenance infusion 1g of aminophylline is added to 1 litre of normal saline to give a solution of 1 mg/ml.
dose: 500-700mcg/kg/hour. If elderly: 300mcg/kg/hour
plasma theophylline concentrations should be monitored
WHat does a respiratory picture look like on ABG?
RO ME
Respiratory = Opposite
low pH + high PaCO2 i.e. acidosis, or
high pH + low PaCO2 i.e. alkalosis
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)
What does a metabolic picture look like on ABG?
Metabolic = Equal
low pH + low bicarbonate i.e. acidosis, or
high pH + high bicarbonate i.e. akalosis
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)
What does this show?
Pleural plaques
What are the asbestosis related damage?
Pleural plaques
Pleural thickening
Asbestosis
Mesothelioma
What are the features of asbestosis ?
latent period is typically 15-30 years.
Typically fibrosis of lower lobes
dyspnoea and reduced exercise tolerance
clubbing
bilateral end-inspiratory crackles
lung function tests show a restrictive pattern with reduced gas transfer
What spirometry pattern is there in asbestosis ?
Restrictive picture
Reduced gas transfer
How do you manage asbestosis ?
Conservatively
How do you manage asbestosis ?
Conservatively
What is the most dangerous form of asbestos?
Crocodile blue
What is the prognosis of mesothelioma?
8-14 months
What is the most common form of cancer from asbetos?
Lung cancer
Then Mesothelioma
Smoking has a synergistic effect with asbestos
What bacteria are typically implicated in aaspiration pneumonia?
Streptococcus pneumoniae
Staphylococcus aureus
Haemophilus influenzae
Pseudomonas aeruginosa
Klebsiella: often seen in aspiration lobar pneumonia in alcoholics
Bacteroides
Prevotella
Fusobacterium
Peptostreptococcus
How should asthma be diagnosed?
patients should be asked if their symptoms are better on days away from work/during holidays. If so, patients should be referred to a specialist as possible occupational asthma
all patients should have spirometry with a bronchodilator reversibility (BDR) test
all patients should have a FeNO test
WHat does a FeNO > 40 suggest?
in adults level of >= 40 parts per billion (ppb) is considered positive
in children a level of >= 35 parts per billion (ppb) is considered positive
What FEV1 and FVC is seen in asthma?
Obstructive picture
FEV1 reduced
FVC reduced, but not as much as FEV1
FEV1/FVC ratio: < 70% is OBSTRUCTIVE
What is considered positive reversibility test?
Adults: improvement in FEV1 of 12% or more and increase in volume of 200 ml or more
Children: positive test is indicated by an improvement in FEV1 of 12% or more
What is the treatment algorhythm for asthma?
- SABA
- SABA + ICS
- SABA + ICS + Leuotrine receptor antagonist
(continue leukotrine receptor antagonist based on response) - SABA + ICS + LABA
- SABA + Switch to MART (ICS/LABA)
- SABA + Medium MART
- SABA + High dose ICS ( not mart) + Theophylline
What is the mechanism of theophylline ?
Long term muscarinic antagonist
What is MART therapy?
Combination of ICS and LABA
What is the definitions of low, medium and high dose ICS?
<= 400 micrograms budesonide or equivalent = low dose
400 micrograms - 800 micrograms budesonide or equivalent = moderate dose
> 800 micrograms budesonide or equivalent= high dose.
Exposure to what is likely to cause occupational asthma?
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
Management: Refer to specialist
What is atelectasis ?
Airways obstructed from bronchial secretions
What are the features of atelectasis ? Management?
dyspnoea and hypoxaemia around 72 hours postoperatively
- Sit upright
- Breathing exercises
What are people who work in aerospace or fluorescent light bulbs/golf-club heads?
Beryliosis
Features of beryliosis?
lung fibrosis - Lower lobe fibrosis
bilateral hilar lymphadenopathy
What does tram track and signet rings suggest ?
Bronchiectasis
What is seen on this CT?
Bronchiectasis
What are the causes of bronchiectasis?
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
Indications for chest drain?
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
Contrainidcations to chest drain?
INR > 1.3
Platelet count < 75
Pulmonary bullae
Pleural adhesions
How to insert a chest drain?
- Position at 45 degrees
- 5’th intercostal space - mid axillary line
- Seldeinger technique
- Stitch drain in
- Ensure swinging and bubbling
Where is a chest drain inserted?
inserted into the pleural cavity which creates a one-way valve, allowing movement of air or liquid out of the cavity.
How to treat bronchiectasis?
Physical training
Antibiotics for exacerbation
Rotating antibiotics for severe cases
Immunisation
Consideration for surgery for localised cases
What bacteria as associated with bronchiectasis exacerbation ?
Haemophilus influenzae (most common)
Pseudomonas aeruginosa
Klebsiella spp.
Streptococcus pneumoniae
What is the most likely cause of bronchiolitis?
RSV
What is re-expansion pulmonary oedema? How is it prevented?
Rapid chest drain drainage
Do not allow more than 1.5 L to drain in first sitting
Drain 500 ml, then clamp for one hour. Then repeat
Indications for removing chest drain?
No output for > 24 hours
In pneumothorax: When drain no longer bubbling
Causes of caveatting lung lesion ?
abscess (Staph aureus, Klebsiella and Pseudomonas)
squamous cell lung cancer
tuberculosis
Wegener’s granulomatosis
pulmonary embolism
rheumatoid arthritis
aspergillosis, histoplasmosis, coccidioidomycosis
Causes of coin lesions?
malignant tumour: lung cancer or metastases
benign tumour: hamartoma
infection: pneumonia, abscess, TB, hydatid cyst
AV malformation
Causes of lobar collapse?
lung cancer (the most common cause in older adults)
asthma (due to mucous plugging)
foreign body
Features of lobar collapse on chest X-ray?
Tracheal deviation towards the side of the collapse
Mediastinal shift towards the side of the collapse
Elevation of the hemidiaphragm
What cancers commonly metastasise to lung?
breast cancer
colorectal cancer
renal cell cancer
bladder cancer
prostate cancer
What cancers cause cannon ball metastasis?
Renal carcinoma
Prostatic cancer
Choriocarcinoma
Features of pulmonary oedema?
interstitial oedema
bat’s wing appearance
upper lobe diversion (increased blood flow to the superior parts of the lung)
Kerley B lines
pleural effusion
cardiomegaly may be seen if there is cardiogenic cause
What are these?
Kerley lines
Blue is Kerley B lies ( periphery) - seen in pulmonary oedema
What causes opacification on CXR?
consolidation
pleural effusion
collapse
pneumonectomy
specific lesions e.g. tumours
fluid e.g. pulmonary oedema
Causes of white out + trachea pulled towards?
Pneumonectomy
Complete lung collapse e.g. endobronchial intubation
Pulmonary hypoplasia
Causes of white out + trachea central?
Consolidation
Pulmonary oedema (usually bilateral)
Mesothelioma
Causes of white out + trachea pushed away?
Pleural effusion
Diaphragmatic hernia
Large thoracic mass
Causes of COPD?
Smoking!
Alpha-1 antitrypsin deficiency
Other causes
cadmium (used in smelting)
coal
cotton
cement
grain
Features of COPD?
Cough: often productive
Dyspnoea
Wheeze
In severe cases, right-sided heart failure may develop resulting in peripheral oedema
How is the severity of COPD worked out?
FEV1
(By definition will also have FEV1/FVC < 70%)
If the FEV1 is greater than 80% predicted but the post-bronchodilator FEV1/FVC is < 0.7 then this is classified as Stage 1 - mild
Who should be considered for LTOT?
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
What criteria should be met to offer
?
Offer LTOT to patients with 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
What general things should be done for management of COPD?
Pneumococcal vaccine
Influenza vaccine
Smoking cessation
Pulmonary rehab
First line management in stable COPD?
- SABA or SAMA
- Consider reversible asthma element
No asthma:LABA + LAMA
if already taking a SAMA, discontinue and switch to a SABA
Asthma component:
LABA + inhaled corticosteroid (ICS)
if patients remain breathless or have exacerbations offer triple therapy i.e. LAMA + LABA + ICS
- Oral theophylline
How to determine if COPD has a asthma component?
a higher blood eosinophil count - note that NICE 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%)
Who should be considered for prophylactic antibiotics in COPD?
Patients should not smoke, have optimised standard treatments and continue to have exacerbations
CT thorax (to exclude bronchiectasis) and sputum culture (to exclude atypical infections and tuberculosis)
LFTs and an ECG to exclude QT prolongation should also be done as azithromycin can prolong the QT interval
Management of COPD + Cor Pulmonale ?
Loop diuretic for oedema, consider long-term oxygen therapy
What are the features of Cor Pulmonale ?
Peripheral oedema
Raised jugular venous pressure,
Systolic parasternal heave
Loud P2
What improves COPD prognosis?
smoking cessation - the single most important intervention in patients who are still smoking
long term oxygen therapy in patients who fit criteria
lung volume reduction surgery in selected patients
What antibiotic should be considered for COPD prophylaxis?
Azithromycin
Side effect of azithormycin?
LFTs and an ECG to exclude QT prolongation should also be done as azithromycin can prolong the QT interval
Features of cystic fibrosis?
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
General management of cystic fibrosis?
High calorie diet
Prevent getting pseudomonas and Burkholderia
Vitamin supplements
Pancreatic enzyme
What is a strong contraindication to lung transplant in CF?
chronic infection with Burkholderia cepacia is an important CF-specific contraindication to lung transplantation
Treatment for F508 CF?
Lumacaftor/Ivacaftor (Orkambi)
What type of drug is theophylline?
Non-specific inhibitor of phosphodiesterase resulting in an increase in cAMP
Methylxanthine
What type of disease is eosinophilic granulomatosis with polyangiitis (Churg-Strauss syndrome)
pANCA
small-medium vessel vasculitis.
Features of Churg Strauss?
asthma
blood eosinophilia (e.g. > 10%)
paranasal sinusitis
mononeuritis multiplex
pANCA positive in 60%
What type of hypersensitivity reaction is extrinsic allergicic alveoli’s?
Type III hypersensitivity (mostly)
type 4 also has a part to play
Examples of extrinsic allergic alveoli’s?
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*
Presentation of extrinsic allergic alevolitis?
acute (occurs 4-8 hrs after exposure)
- dyspnoea
- dry cough
- fever
chronic (occurs weeks-months after exposure)
- lethargy
- dyspnoea
- productive cough
- anorexia and weight loss
Where is the fibrosis in EAA?
Upper lobes
Investigation findings of EAA?
imaging: upper/mid-zone fibrosis
bronchoalveolar lavage: lymphocytosis
serologic assays for specific IgG antibodies
blood: NO eosinophilia
Is there an eosinophilia in EAA?
NO NO NO
Management of EAA?
- Glucocorticoidds
- Avoid precipitating factors
What are the features of granulomatosis polyangitis?
Upper respiratory tract: epistaxis, Sinusitis, nasal crusting
Lower respiratory tract: dyspnoea, Haemoptysis
rapidly progressive glomerulonephritis (‘pauci-immune’, 80% of patients)
saddle-shape nose deformity
also: vasculitic rash, eye involvement (e.g. proptosis), cranial nerve lesions
cANCA
Investigating findings of Wegenrs?
cANCA positive in > 90%, pANCA positive in 25%
chest x-ray: wide variety of presentations, including cavitating lesions
renal biopsy: epithelial crescents in Bowman’s capsule
Management of Wegners?
steroids
cyclophosphamide (90% response)
plasma exchange
median survival = 8-9 years
What is histoplasmosis?
Histoplasma capsulatum. It is most commonly encountered in the Mississippi and Ohio River valleys.
Features of histoplasmosis?
URTI symptoms
retrosternal pain
Management of histoplasmosis?
amphotericin or itraconazole are the pharmacological agents of choice for histoplasmosis
Features of idiopathic pulmonary fibrosis?
progressive exertional dyspnoea
bibasal fine end-inspiratory crepitations on auscultation
dry cough
clubbing
What type of spirometry picture do you see in pulmonary fibrosis?
Restrictive picture
impaired gas exchange: reduced transfer factor (TLCO)
What imaging finding do you see in pulmonary fibrosis?
bilateral interstitial shadowing (typically small, irregular, peripheral opacities - ‘ground-glass’ - later progressing to ‘honeycombing’) may be seen on a chest x-ray but high-resolution CT scanning is the investigation of choice and required to make a diagnosis of IPF
Management of pulmonary fibrosis?
pirfenidone (an antifibrotic agent)
Features of Kartenagers syndrome?
dextrocardia or complete situs inversus
bronchiectasis
recurrent sinusitis
subfertility (secondary to diminished sperm motility and defective ciliary action in the fallopian tubes)
What is the gram stain of Klebsielta?
Gram negative
- Typically following aspiration
Presentation of Klebsiella pneumonia?
more common in alcoholic and diabetics
may occur following aspiration
‘red-currant jelly’ sputum
often affects upper lobes
What is Lofgren’s syndrome ?
acute form sarcoidosis characterised by bilateral hilar lymphadenopathy (BHL), erythema nodosum, fever and polyarthralgia.
What is the most likely cause of lung abscess?
Secondary to aspiration pneumonia
Other causes:
direct extension e.g. from an empyema
bronchial obstruction e.g. secondary from a lung tumour
What on mono microbial cause of lung abscess?
Staphylococcus aureus
Klebsiella pneumonia
Pseudomonas aeruginosa
Signs of lung abscess?
Systemic symptoms of night sweats
Subacute onset
Possible finger clubbing
Foul smelling sputum
chest x-ray
fluid-filled space within an area of consolidation
an air-fluid level is typically seen
sputum and blood cultures should be obtained
What type of lung cancer gives you hoarseness?
Pancoast tumours
Paraneoplastic effect of a small cell lung cancer?
ADH
ACTH - not typical, hypertension, hyperglycaemia, hypokalaemia, alkalosis and muscle weakness are more common than buffalo hump etc
Lambert-Eaton syndrome
Paraneoplastic effect of a squamous cell lung cancer?
Parathyroid hormone-related protein (PTH-rp) secretion causing hypercalcaemia
Clubbing
Hypertrophic pulmonary osteoarthropathy (HPOA)
hyperthyroidism due to ectopic TSH
Paraneoplastic effect of adenocarcinoma?
Gynaecomastia
Hypertrophic pulmonary osteoarthropathy (HPOA)
What blood changes can be seen FBC?
Thrombocytosis
Investigations for lung cancer?
- CXR
- CT thorax
- Bronchoscopy - biopsy
- PET scan
What lung cancer should receive aPET scan?
Non- small cell lung cancer
What are the types of non-small cell lung cancer?
Squamous
Adenocarcinoma
Large cell
Management of non-small cell lung cancer?
- Lobectomy - in stage I and II cancer ( first line) curative intent
- Radiotherapy ( stage I - III) curative intent
- Chemotherapy non-curative
Complete resection: Offer chemotherapy adjuvant
Incomplete resection: Offer radiotherapy +/- chemotherapy
What chemotherapy is used for non-small lung cancer?
Third-generation chemotherapy agent: e.g. docetaxel, paclitaxel or gemcitabine
Platinum agent: e.g. carboplatin or cisplatin
Management of stage I-III NSLC, not fit for surgery?
Offer chemoradiotherapy
What is considered extensive small cell lung cancer?
T 1-4, N 0-3, M1
What is considered limited small cell lung cancer?
T 1-4, N 0-3, M0
Treatment for limited small cell lung cancer?
4-6 cycles of Cisplatin-based combination chemotherapy
Concurrent or adjunct thoracic radiotherapy is only considered if there has been a good response to chemotherapy
Treatment for extensive small cell lung cancer?
Platinum-based combination therapy where the patient is reassessed for a response after each cycle (up to a maximum of 6 cycles)
Concurrent or adjunct thoracic radiotherapy can be considered if there has been a good response to chemotherapy at both the primary and metastatic sites.
How to treat relapse of small cell lung cancer?
Further chemotherapy (maximum 6 cycles)
Palliative radiotherapy to control local symptoms
Local metastasis of lung cancer?
Nerve palsy; superior vena cava obstruction and pericarditis
Metastatic sites for lung cancer?
Brain, spinal cord, bone, liver and adrenal glands are common sites
Contraindications to surgery in lung cancer?
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
When should you offer a CXR for lung cancer?
40 and over if they have 2 or more of the following unexplained symptoms, or if they have ever smoked and have 1 or more of the following unexplained symptoms:
cough
fatigue
shortness of breath
chest pain
weight loss
appetite loss
What cells does small cell lung cancer arise from?
APUD cells
Amine - high amine content
Precursor Uptake - high uptake of amine precursors
Decarboxylase - high content of the enzyme decarboxylase
Features of small cell lung cancer?
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
Causes of upper zone fibrosis?
C - Coal worker’s pneumoconiosis
H - Histiocytosis/ hypersensitivity pneumonitis
A - Ankylosing spondylitis
R - Radiation
T - Tuberculosis
S - Silicosis/sarcoidosis
Causes of lower zone fibrosis?
idiopathic pulmonary fibrosis
most connective tissue disorders (except ankylosing spondylitis) e.g. SLE
drug-induced: amiodarone, bleomycin, methotrexate
asbestosis
What type of cancer is a mesothelioma?
Cancer of the mesothelium of the pleura
Features of mesothelioma?
Dyspnoea, weight loss, chest wall pain
Clubbing
30% present as painless pleural effusion
Only 20% have pre-existing asbestosis
History of asbestos exposure in 85-90%, latent period of 30-40 years
What does mesothelioma look up on CXR?
Pleural thickening
Pleural effusion
Features of microscopic polyangitis?
renal impairment: raised creatinine, haematuria, proteinuria
fever
other systemic symptoms: lethargy, myalgia, weight loss
rash: palpable purpura
cough, dyspnoea, haemoptysis
mononeuritis multiplex
What is microscopic polyangitis?
pANCA (against MPO) - positive in 50-75%
cANCA (against PR3) - positive in 40%
What is a microscopic polangitis?
small-vessel ANCA vasculitis.
What causes Middle Eastern respiratory syndrome?
betacoronavirus MERS-CoV.
Features of obesity hypoventilation syndrome?
Sleep apnoea
Morning headaches
Daytime sleepiness
Reduce exercise tolerance
Risk factors for obesity hypoventilation syndrome?
obesity
macroglossia: acromegaly, hypothyroidism, amyloidosis
large tonsils
Marfan’s syndrome
Consequences: daytime somnolence
compensated respiratory acidosis
hypertension
Assessment of sleepiness?
Epworth Sleepiness Scale - questionnaire completed by patient +/- partner
Multiple Sleep Latency Test (MSLT) - measures the time to fall asleep in a dark room (using EEG criteria)
Diagnostic test for sleep apnoea ?
sleep studies (polysomnography) - ranging from monitoring of pulse oximetry at night to full polysomnography where a wide variety of physiological factors are measured including EEG, respiratory airflow, thoraco-abdominal movement, snoring and pulse oximetry
Management of sleep apnoea?
weight loss
continuous positive airway pressure (CPAP) is first line for moderate or severe OSAHS
intra-oral devices (e.g. mandibular advancement) may be used if CPAP is not tolerated or for patients with mild OSAHS where there is no daytime sleepiness
the DVLA should be informed if OSAHS is causing excessive daytime sleepiness
limited evidence to support use of pharmacological agents
What is considered an obstructive picture?
FEV1/FVC < 80%
What is considered a restrictive picture?
FEV1/FVC > 80%
Examples of obstructive pictures?
Chronic obstructive pulmonary disease
chronic bronchitis
emphysema: including alpha-1 antitrypsin deficiency
Asthma
Bronchiectasis
Examples of restrictive pictures?
Intrapulmonary:
idiopathic pulmonary fibrosis
extrinsic allergic alveolitis
coal worker’s pneumoconiosis/progressive massive fibrosis
silicosis
sarcoidosis
histiocytosis
drug-induced fibrosis: amiodarone, bleomycin, methotrexate
asbestosis
Extrapulmonary:
neuromuscular disease: polio, myasthenia gravis
obesity
scoliosis
Causes of transudate pleural effusion?
heart failure (most common transudate cause)
hypoalbuminaemia
- liver disease
- nephrotic syndrome
- malabsorption
hypothyroidism
Meigs’ syndrome
Definition of exudates?
> 30
Definition of transudates?
<30
Light’s criteria should be applied when?
Protein level is 25-35
What are the rules of Light’s criteria?
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
Pleural effusions with a low glucose?
Rheumatoid arthritis
Tuberculosis
Pleural effusions with raised amylase?
Pancreatitis
Oesophageal perforation
Pleural effusions with heavy blood staining?
Mesothelioma
Pulmonary embolism
Tuberculosis
When infection in expected in pleural effusion ? How is this managed?
pH < 7.2
Turbid colour
In such situation - insert chest drain
Pneumonia + Herpes libilais ?
Strep pneumonia
Pneumonia + COPD
Haemophilus
Pneumonia + recent influenza infection?
Staph aureus
Pneumonia + dry cough + autoimmune haemolytic anaemia + Erythema multiform ?
Mycoplasma
Pneumonia + hyponatraemia +lymphopaenia
Legionella
Pneumonia + alcoholic?
Klebsiella
CURB 65
Confusion
Urea > 7
Respiratory rate > 30
Blood pressure < 90 mmHg
65
home-based care for patients with a CRB65 score of 0
oral amoxicillin is generally used first-line
hospital assessment for all other patients, particularly those with a CRB65 score of 2 or more.
GP practice remove the urea
Resolution from pneumonia?
1 week Fever should have resolved
4 weeks Chest pain and sputum production should have substantially reduced
6 weeks Cough and breathlessness should have substantially reduced
3 months Most symptoms should have resolved but fatigue may still be present
6 months Most people will feel back to normal.
For pneumonia, when should a CXR be repeated?
6 Weeks
Risk factors for a pneumothorax?
Pre-existing lung disease
Non-invasive ventilation
Connective tissue disease: Marfans, rheumatoid arthritis
Management of primary pneumothorax?
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
Management of secondary pneumothorax?
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.
otherwise aspiration should be attempted if the rim of air is between 1-2cm. If aspiration fails (i.e. pneumothorax is still greater than 1cm) a chest drain should be inserted. All patients should be admitted for at least 24 hours
if the pneumothorax is less the 1cm then the BTS guidelines suggest giving oxygen and admitting for 24 hours
When can you fly post pneumothorax?
Yes - checked with CXR one week post
Pulmonary function testing: obstructive?
FEV1 - significantly reduced
FVC - reduced or normal
FEV1% (FEV1/FVC) - reduced
Pulmonary function testing: restrictive?
FEV1 - reduced
FVC - significantly reduced
FEV1% (FEV1/FVC) - normal or increased
Obstructive lung disease?
Asthma
COPD
Bronchiectasis
Bronchiolitis obliterans
Restrictive lung disease?
Pulmonary fibrosis
Asbestosis
Sarcoidosis
Acute respiratory distress syndrome
Infant respiratory distress syndrome
Kyphoscoliosis e.g. ankylosing spondylitis
Neuromuscular disorders
Severe obesity
What is diagnostic if pulmonary hypertension?
pulmonary arterial pressure of greater than 25 mmHg at rest
Group 1 pulmonary hypertension?
Group 1: Pulmonary arterial hypertension (PAH)
- idiopathic*
- familial
- associated conditions: collagen vascular disease, congenital heart disease with systemic to pulmonary shunts, HIV**, drugs and toxins, sickle cell disease
- persistent pulmonary hypertension of the newborn
Group 2 pulmonary hypertension?
Group 2: Pulmonary hypertension with left heart disease
- left-sided atrial, ventricular or valvular disease such as left ventricular systolic and diastolic dysfunction, mitral stenosis and mitral regurgitation
Group 3 pulmonary hypertension?
Group 3: Pulmonary hypertension secondary to lung disease/hypoxia
- COPD
- interstitial lung disease
- sleep apnoea
- high altitude
What is group 4 pulmonary hypertension?
Group 4: Pulmonary hypertension due to thromboembolic disease
Causes of respiratory acidosis?
COPD
Decompensation in other respiratory conditions e.g. life-threatening asthma / Pulmonary oedema
Neuromuscular disease
Obesity hypoventilation syndrome
Sedative drugs: benzodiazepines, opiate overdose
Causes of respiratory alkalosis?
Anxiety leading to hyperventilation
Pulmonary embolism
Salicylate poisoning*
CNS disorders: stroke, subarachnoid Haemorrhage, encephalitis
Altitude
Pregnancy
Acidosis and alkalosis in salicylate overdose? - why?
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
What is tidal volume?
volume inspired or expired with each breath at rest
500ml in males, 350ml in females
What is inspiratory reserve volume?
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
What is expiratory reserve volume?
Expiratory reserve volume (ERV) = 750ml
maximum volume of air that can be expired at the end of a normal tidal expiration
What is residual reserve volume?
Residual volume (RV) = 1.2L
volume of air remaining after maximal expiration
increases with age
RV = FRC - ERV
What is functional residual capacity?
Functional residual capacity (FRC)
the volume in the lungs at the end-expiratory position
FRC = ERV + RV
What is vital capacity?
Vital capacity (VC) = 5L
maximum volume of air that can be expired after a maximal inspiration
4,500ml in males, 3,500 mls in females
decreases with age
VC = inspiratory capacity + ERV
What is total lung capacity /
Total lung capacity (TLC) is the sum of the vital capacity + residual volume
What are respiratory complications of rheumatoid?
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
What is Caplan’s syndrome?
Caplan’s syndrome - massive fibrotic nodules with occupational coal dust exposure
Features of sarcoidosis?
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)
What is lofgren’s syndrome ?
Lofgren’s syndrome is an acute form of the disease characterised by bilateral hilar lymphadenopathy (BHL), erythema nodosum, fever and polyarthralgia. It usually carries an excellent prognosis
What is Mikulicz syndrome?
enlargement of the parotid and lacrimal glands due to sarcoidosis, tuberculosis or lymphoma
What is Heerfordt’s syndrome
(uveoparotid fever) there is parotid enlargement, fever and uveitis secondary to sarcoidosis
Chest xray staging for sarcoid?
stage 0 = normal
stage 1 = bilateral hilar lymphadenopathy (BHL)
stage 2 = BHL + interstitial infiltrates
stage 3 = diffuse interstitial infiltrates only
stage 4 = diffuse fibrosis
Spirometry testing for sarcoid?
restrictive
Investigation findings in sarcoid?
spirometry: may show a restrictive defect
tissue biopsy: non-caseating granulomas
gallium-67 scan - not used routinely
the Kveim test (where part of the spleen from a patient with known sarcoidosis is injected under the skin) is no longer performed due to concerns about cross-infection
What are the indications of treatments in sarcoid?
patients with chest x-ray stage 2 or 3 disease who are symptomatic.
hypercalcaemia
eye, heart or neuro involvement
What are the radiograph findings of silicosis?
upper zone fibrosing lung disease
‘egg-shell’ calcification of the hilar lymph nodes
Guidance for a nodule < 5 mm?
clear benign features, or unsuitable for treatment: can be discharged
Guidance for nodule > 8 mm and high risk features?
then CT-PET, and if CT-PET shows high uptake then biopsy
Guidance for > 8mm and low risk features?
then CT surveillance
Subglottic stenosis?
Subglottic stenosis may be defined as a narrowing of the airway below the vocal cords (subglottis) and above the trachea. It may be congenital or acquired.
Mechanism of theophylline?
Xanthine
Mechanism uncertain
non-specific inhibitor of phosphodiesterase resulting in an increase in cAM
Features of theophylline poisoning/
acidosis, hypokalaemia
vomiting
tachycardia, arrhythmias
seizures
Management of theophylline poisoning?
consider gastric lavage if <1 hour prior to ingestion
activated charcoal
whole-bowel irrigation can be performed if theophylline is sustained release form
charcoal haemoperfusion is preferable to haemodialysis
Conditions with raising TLCO / KCO (transfer factor)
asthma
pulmonary haemorrhage (Wegener’s, Goodpasture’s)
left-to-right cardiac shunts
polycythaemia
hyperkinetic states
male gender, exercise
Conditions with low TLCO / KCO
(transfer factor)
pulmonary fibrosis
pneumonia
pulmonary emboli
pulmonary oedema
emphysema
anaemia
low cardiac output
Most common lung cancer in adolescents?
Carcinoid tumour
What causes hypertrophic pulmonary osteoarthropathy?
Squamous cell carcinoma
Causes symmetrical joint tenderness - e.g. wrists
What one bacteria is the worst prognosis for CF?
Bukerholdia
Presentation of Lymphangioleiomyomatosis (LAM) ?
Premenopausal women
proliferation of atypical smooth muscle cells in the lungs, lymphatics and uterus, most likely caused by oestrogens
Presentation is with dyspnoea due to progressive interstitial lung disease, pneumothorax or chylous pleural effusion.
Management of Lymphangioleiomyomatosis (LAM) ?
Medroxyprogesterone is an anti-oestrogen
How do you determine between pseudochylothroax vs chylothorax?
Triglyceride
What monoclonal antibody can be used in asthma with an elevated eosinophilia?
Mepolizumab may be used for asthma with high eosinophils
Used at end of all other options
Management of loeffler syndrome?
Mendazole
Management of pulmonary fibrosis?
Pirfenidone ( antifibrotic agent)
very few medications have been shown to give any benefit in IPF. There is some evidence that pirfenidone (an antifibrotic agent) may be useful in selected patients
When do you put a chest drain in a secondary pneumothorax?
If a secondary pneumothorax > 2cm and/or the patient is short of breath then patient should be treated with chest drain (not aspiration) as first-line
Management of a primary pneumothorax?
- 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 (regardless of size) - if this fails (defined as > 2 cm or still short of breath) then a chest drain should be inserted
How do you manage a patient needing LTOT, who retains CO2?
LTOT with notruanl BIPAP
Pleural effusion: exudate + low glucose + SOB?
Think cancer
Bronchial carcinoma
Presentation of bronchopulmonary fistula?
Large right sided effusion
Constant bubbling in underwater seal
Pleural effusion and a suitable site is marked. A chest drain is inserted without complication and the drain yields frank pus
How does theophylline poisoning affect the heart?
increased myocardial contractility
Other: hypokalaemia, hyperglycaemia, tachycardia and increased myocardial contractility
What increases the risk of tuberculosis ?
Silicosis
What can lead to excessive lacticaemia in asthma
Salbutamol type B lactic acidosis (that is not caused by tissue hypoperfusion or hypoxia resulting in anaerobic metabolism).
Side effect of nicotine replacement therapy?
nausea & vomiting, headaches and flu-like symptom
How should you prescribe nicotine replacement therapy?
Dual method
Patches + (gum lozenges, or another form )
What is the mechanism of varenicline?
Partial nicotinic receptor antagonist
started 1 week before the patients target date to stop
recommended course of treatment is 12 weeks (but patients should be monitored regularly and treatment only continued if not smoking)
Side effect of varenicline?
Nausea ( most common)
headache, insomnia, abnormal dreams
When should varenicline be used with caution?
When has a history of depression / self harm
Mechanism of buproprion?
norepinephrine and dopamine reuptake inhibitor, and nicotinic antagonist
Contraindications for bupropion?
Epilepsy
Breast feeding
Pregnancy
What is fist line smoking cessation in pregnancy?
- CBT
- Nicotine replacement therapy
as mentioned above, varenicline and bupropion are contraindicated
When should Romuflast be used in COPD?
When trial of LAMA + ICS + LABA + SABA used
FEV1 < 50% of predicted
What are the indications for LTOT therapy?
- Resting PaO2 ≤7.3 kPa
- Resting PaO2 ≤8 kPa with evidence of peripheral oedema, polycythaemia (haematocrit ≥55%) or pulmonary hypertension.
What mechanism is mepolizumab and what it’s indication?
IL 5 antagonist
Used in asthma with eosinophilia
When can you use a tyrosine kinase inhibitor in idiopathic pulmonary fibrosis?
a) The person has a forced vital capacity (FVC) between 50% and 80% of predicted
b) The company provides nintedanib with the discount agreed in the patient access scheme and
c) Treatment is stopped if the disease progresses (a confirmed decline in percent predicted FVC of 10% or more) in any 12month period.
What drug prevents acute mountain sickness?
Acetazdolamiode
What are contraindications to NIV?
Recent facial or upper airway surgery or facial injuries.
- Recent upper gastrointestinal surgery.
- Confusion/agitation.
- Bowel obstruction.
- Upper airway obstruction.
- Excessive upper airway secretions.
- Patient actively vomiting.
When should omalizumab be used?
Ongoing frequent symptoms despite treatment, including a recent exacerbation
Symptoms are worse outdoors in the summer months
History of atopy
Elevated IgE levels
When should omalizumab be used?
Ongoing frequent symptoms despite treatment, including a recent exacerbation
Symptoms are worse outdoors in the summer months
History of atopy
Elevated IgE levels
COPD + reversible asthma component?
LABA + ICS
What are Kelley B lines?
1-2 cm diagonal lines at the very periphery
Means pulmonary oedema
Empyema vs abscess?
Empyema is an accumulation of pus in the pleural space, the cavity between the lungs and the inner surface of the chest wall
How to determine if pleural aspirate if from an empyema?
If the pleural fluid is turbid or milky it should becentrifuged.
If the supernatant (liquid which lies above the sediment) is clear, the turbid fluid was due to cell debris and empyema is likely
Tests that need to be done for LTOT?
- ABG
- ECHO - evidence of pulmonary hypertension
Consolidation above horizontal fissure?
Upper lobe
Consolidation below horizontal fissure?
Below lobe
Beta D Glucan + Missippi ( or bats) + URTI symptoms
retrosternal pain or acute respiratory failure ?
Histoplasmosis
What are the causes of bulging fissure sign?
Klebsiella pneumonia
What is the mechanism of thunderstorm asthma?
Sudden pollen and spore release due to pressure changes
What is a common P450 inducer in COPD patients?
Smoking
What is see on this CXR ?
Pleural thickening
Missippi ?
Think histoplasmosis
Management of histoplasmosis ?
Itraconazole
cANCA +ve
pANCA +ve
Crescentic renal stuff
No nose changes ?
Microscopic polangitis
What type of ABG do you see in untreated OSA or obesity hypoventilation syndrome?
Compensated respiratory acidosis
Difference between Wegners and Churg Strauss?
Renal failure –> Wegners
Epistaxis –> wegners
cANCA –> wegners
Asthma –> Churg strauss
pANCA –> Churg strauss
Eosinophillia –> Churg struass
What medication may precipitate churg struass?
LTRA
Symtomatic primary pneumothorax < 2cm - management?
As SOB pleural aspiration
Acute complication of NIV?
pneuomothoax
Management of weighers?
Cyclophosphamide + steroids
COPD: >2 exacerbations per year + FEV1<50%? what medication to add?
Roflumilast
parenchymal bands, traction bronchiectasis and honeycomb lung?
Asbestosis
Causes of simple pulmonary eosinophilia?
Ascaris lumbricoides, Strongyloides, or Ancylostoma
Causes of pulmonary eosinophilia?
roundworms Wuchereria bancrofti or Brugia malayi, common in the Asian Subcontinent and Africa
Spread by mosquito
can cause elephantiasis
paroxysmal nocturnal cough, wheeze, and breathlessness
Management of tropical pulmonary eosinophilia?
diethylcarbamazine for diagnosis and, which is also the main treatment.
Stable COPD treatment pathway?
Prodrome of chlamydia psittaci?
diarrhoea
epistaxis
high fevers
Splenomegaly
Low white blood cell count are common
What is the other name for extrinsic allergic alveolitis?
Hypersensitivity pneumonitis
Pseudomonas eradication in CF patient?
IV ceftazidime + nebulised tobramycin
What is the poor prognostic factor for asbestosis?
FINGER CLUBBING
mononeuritis multiplex causes?
vasculitis
diabetes
AIDS
amyloidosis
rheumatoid arthritis.
Treatment for small cell lung cancer ?
What type of kidney damage is seen on charge Strauss?
pauci immune crescentic glomerulonephritis
Most useful marker to determine if haemothorax?
If the haematocrit of the pleural fluid is more than half of the patient’s peripheral blood haematocrit, the patient has a haemothorax
causes of exudate effusions?
infection
pneumonia (most common exudate cause),
tuberculosis
subphrenic abscess
connective tissue disease
rheumatoid arthritis
systemic lupus erythmatosus
neoplasia
lung cancer
mesothelioma
metastases
pancreatitis
pulmonary embolism
Dressler’s syndrome
yellow nail syndrome
Difference between aspergilloma and invasive aspergillosis ?
aspergilloma fungus ball
Invasive aspergillosis - syndrome, invasion of fungi and invasive of vessel with blood in sputum
What does this show?
g sub-pleural reticular opacities that increase from the apex to the bases of the lungs.
Pulmonary fibrosis
Mechanism of Omalizumab?
Anti- IgE
Pneumothorax diving advice?
Do not drive unless get pleurodesis
Pneumothorax flying advice?
may travel 2 weeks after successful drainage if there is no residual air. The British Thoracic Society used to recommend not travelling by air for a period of 6 weeks but this has now been changed to 1 week post check x-ray
Secondary pneumothorax <1 cm management?
Admit for 24 hours, oxygen and review
What is this?
Mesothelioma
Best diagnostic test for bronchiectasis ?
HRCT
When should CXR repeat be done?
6 weeks
What is suggestive of NSAID sensitive asthma?
Presence of nasal polyps
Empyema + chest drain is bubbling. This bubbling is more significant when the patient is asked to cough.
Bronchopleural fistula
Drugs that cause pleural effusions?
Nitrofurantoin
Amiodarone
Methotrexat
What causes usual interstial pneumonia
UIP is scan finding not diagnosis
Idiopathic pulmonary fibrosis
Asbestosis
EAA
Differentiating between EAA and idiopathic pulmonary fibrosis?
occurrence of episodic dyspnoea, cough, and flu-like symptoms in response to an environmental antigen is consistent with the acute presentation of hypersensitivity pneumonitis. Patients are well in between episodes and during the early phase of the disease examination and investigation can be normal.
History of worsening asthma post intubation?
Think posterior supraglotic stenosis
What does the PO2 have to be for consider LTOT?
<8
How does wegners present on CT scan?
few well-defined regions of airspace opacification (as demonstrated by the grey-coloured, round lung markings) which can represent consolidation or pulmonary haemorrhag
Complication of transjugular intrahepatic portosystemic shunt (TIPS)?
Pulmonary hypertension
Test to determine prognosis of idiopathic pulmonary fibrosis?
Carbon moxoside transfer test
Previous TB
Think aspergilloma
Findings that suggest empyema on aspiration?
Turbid / pus
Micro-organisms seen
pH < 7.2
Causes of lower zone fibrosis?
Causes of lower zone fibrosis: MAID
Most connective tissue diseases (e.g. rheumatoid arthritis)
Asbestosis
Idiopathic pulmonary fibrosis, infection
Drugs (e.g. methotrexate, amiodarone, bleomycin)
What type of empysema is seen in alpha 1 antitrypsin disease?
Panacinar emphysema
Hasan assocaited low transfer factor
Best management for anxiety on NIV?
Haloperidol
Management of diabetes in CF?
High calorie diet and insulin
Treatment of ARDS?
Low tidal volume ventilation
After a reassuring aspirate from pleural effusion, what next test should be done to determine aetiology
CT thorax
How does obestiy affect transfer factor ?>
It does not
Pleural thickening best investigation?
VATS
Management of someone who develops type 2 respiratory failure while on LTOT trial?
may have clinically unstable disease. These patients should undergo further medical optimisation and be reassessed after 4 weeks
How to give nebulises on NIV?
Take off mask, then put back on
Use of oxygen in pneumothorax management?
Exchange of nitrogen for oxygen allowing quicker resorption.
