General Flashcards
What are the features of moderate asthma exacerbation?
PEFR 50-75% best or predicted
Speech normal
RR < 25 / min
Pulse < 110 bpm
What are the features of severe asthma exacerbation
PEFR 33 - 50% best or predicted
Can’t complete sentences
RR > 25/min
Pulse > 110 bpm
What are the features of a lifetheatening asthma attack?
PEFR < 33% best or predicted
Oxygen sats < 92%
‘Normal’ pC02 (4.6-6.0 kPa)
Silent chest, cyanosis or feeble respiratory effort
Bradycardia, dysrhythmia or hypotension
Exhaustion, confusion or coma
What does a normal pCO2 mean in an acute asthma attack?
Exhausation
Treat as life threatening
How many features in the life threatening section need to be present to treat as a life threatening asthma attack?
Any one
Management of acute asthma exacerbation?
Oxygen
Bronchodilation - SABA
Corticosteroid
- 40/50mg predinoslone for 5 days
Ipratroium
IV magnesium sulphate
IV aminophylline
What is the criteria for discharge in asthma attack?
Stable on discharge medication - no nebs or O2 for 12 hours
PEF > 75 % of predicted
Most common organisms causing infective exacerbation of COPD?
Haemophilus influenzae
Streptococcus pneumiae
Moraxella
Antibitoic choice in infective exacerbation of COPD?
Amoxicllin
Clrithromycin
Doxycycline
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)
What are the featues of allergic boronchopulmonary aspergillosis?
bronchoconstriction: wheeze, cough, dyspnoea. Patients may have a previous label of asthma
bronchiectasis (proximal)
Investigations for allergic bronchopulmonary aspergillosis?
eosinophilia
flitting CXR changes
positive radioallergosorbent (RAST) test to Aspergillus
positive IgG precipitins (not as positive as in aspergilloma)
raised IgE
Bronchiectasis + eosinphillia?
Allergic bronchopulmonary aspergillosis
What are the genetics behind alpha-1 antitrypsin deficiency?
Chromosome 14
Autosomal recessive / co-dominant fashion
Normal genotype: PiMM
In alpha 1 antitrypsin how does PiMZ present?
carrier and unlikely to develop emphysema if a non-smoker
In alpha 1 antitrypsin how does PiSS present?
50% A1AT levels
Empysema
Investigations for A1AT?
A1AT concentrations
Spiromtetry: Obstructive
What is the spirometry picture in A1AT deficiency?
Obstructive
Management of A1AT deficiency?
no smoking
supportive: bronchodilators, physiotherapy
intravenous alpha1-antitrypsin protein concentrates
surgery: lung volume reduction surgery, lung transplantation
How can acute mountain sickness (AMS) be treated?
Acetazolimide
- it causes a primary metabolic acidosis and compensatory respiratory alkalosis which increases respiratory rate and improves oxygenation
Gain altitude by no more than 500 meters per day
How to interpret arterial blood gas?
- How is the patient?
- Is the patient hypoxaemic?
the Pa02 on air should be >10 kPa - Is the patient acidaemic (pH <7.35) or alkalaemic (pH >7.45)
- Respiratory component: What has happened to the PaCO2?
PaCO2 > 6.0 kPa suggests a respiratory acidosis (or respiratory compensation for a metabolic alkalosis)
PaCO2 < 4.7 kPa suggests a respiratory alkalosis (or respiratory compensation for a metabolic acidosis) - Metabolic component: What is the bicarbonate level/base excess?
bicarbonate < 22 mmol/l (or a base excess < - 2mmol/l) suggests a metabolic acidosis (or renal compensation for a respiratory alkalosis)
bicarbonate > 26 mmol/l (or a base excess > + 2mmol/l) suggests a metabolic alkalosis (or renal compensation for a respiratory acidosis)
What does Respiratory = opposite mean?
low pH + high PaCO2 i.e. acidosis, or
high pH + low PaCO2 i.e. alkalosis
ROME
What does metabolic = equal mean?
low pH + low bicarbonate i.e. acidosis, or
high pH + high bicarbonate i.e. akalosis
ROME
Types of asbestosis lung disease?
Pleural plaques
Pleural thickening
Asbestosis
Mesothelioma
Lung cancer
How are pleural plaques from asbestosis managed?
Benign
Do not require follow up
What lobe does asbestosis typically affect?
Lower lobe fibrosis
Features of asbestosis ?
dyspnoea and reduced exercise tolerance
clubbing
bilateral end-inspiratory crackles
lung function tests show a restrictive pattern with reduced gas transfer
What is the most dangerous type of asbestos ?
Crocodile blue
Features of mesothelioma?
progressive shortness-of-breath
chest pain
pleural effusion
What is the prognosis of mesothelioma?
8-14 months
What is the most common cancer from asbestosis?
Lung cancer
What type of cancer is mesothelioma?
Malignant disease of the pleura
What test is now done to test for asthma as a diagnosis?
fractional exhaled nitric oxide (FeNO)
Looks for inducible nitric oxide from eosinophils
How is asthma diagnosed in > 17 year olds?
- Better off from work –> specialist referral for occupational asthma
- FeNO on everyone
- Spironometry + bronchodilator reversibility testing
How is asthma diagnosed in children?
- Spirometry
- If spirometry is normal or, obstructive + no bronchodilator reversibility –> FeNO test
What is considered a diagnostic level for FeNO in adults?
in adults level of >= 40 parts per billion (ppb) is considered positive
What is considered a diagnostic level for FeNO in children?
in children level of >= 35 parts per billion (ppb) is considered positive
What is considered an obstructive picture on FEV1 to FVC
70% or less is considered diagnostic
What is considered a positive reversibility test in adults?
n improvement in FEV1 of 12% or more and increase in volume of 200 ml or more
Management of asthma?
- SABA
- SABA + Low dose ICS
- SABA + low-dose ICS + leukotriene receptor antagonist (LTRA)
- SABA + low-dose ICS + long-acting beta agonist (LABA), (LTRA depending on response)
- SABA +/- LTRA - Switch ICS/LABA for a maintenance and reliever therapy (MART), that includes a low-dose ICS
- SABA +/- LTRA + medium-dose ICS MART
- SABA +/- LTRA + one of the following options:
- increase ICS to high-dose (only as part of a fixed-dose regime, not as a MART)
- a trial of an additional drug (for example, a long-acting muscarinic receptor antagonist or theophylline)
What is Maintenance and reliever therapy (MART) for asthma?
combined ICS and LABA treatment
What is a low dose ICS?
< 400 micrograms
What is a medium dose ICS?
400-800 micrograms
What is a high dose ICS?
> 800 micrograms
Causes of 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
What is atelectasis?
postoperative complication in which basal alveolar collapse can lead to respiratory difficulty
Most common causes of bilateral pleural effusion
Sarcoidosis
Tuberculosis
Other causes:
lymphoma/other malignancy
pneumoconiosis e.g. berylliosis
fungi e.g. histoplasmosis, coccidioidomycosis
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
Management of bronchiectasis?
- Physical training
- Antibiotics for exacerbations + long term rotating antibiotics
- Bronchodilator
- Immunisation
Most common organisms for exacerbation in bronchiectasis?
Haemophilus influenzae (most common)
Pseudomonas aeruginosa
Klebsiella spp.
Streptococcus pneumoniae
Causes of bronchiolitis?
RSV (most common)
other causes: mycoplasma, adenoviruses
may be secondary bacterial infection
more serious if bronchopulmonary dysplasia (e.g. Premature), congenital heart disease or cystic fibrosis
Features of bronchiolitis?
coryzal symptoms (including mild fever) precede:
dry cough
increasing breathlessness
wheezing, fine inspiratory crackles (not always present)
feeding difficulties associated with increasing dyspnoea are often the reason for hospital admission
Red flags with bronchiolitis?
apnoea (observed or reported)
child looks seriously unwell to a healthcare professional
severe respiratory distress, for example grunting, marked chest recession, or a respiratory rate of over 70 breaths/minute
central cyanosis
persistent oxygen saturation of less than 92% when breathing air.
Management of bronchiolitis?
coryzal symptoms (including mild fever) precede:
dry cough
increasing breathlessness
wheezing, fine inspiratory crackles (not always present)
feeding difficulties associated with increasing dyspnoea are often the reason for hospital admission
Indications for chest drain insertion?
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
Insertion of chest drain contraindications?
INR > 1.3
Platelet count < 75
Pulmonary bullae
Pleural adhesions
Where should a intercostal chest drain be inserted?
5th intercostal space in the midaxillary line
Causes of cavitating lung lesions?
abscess (Staph aureus, Klebsiella and Pseudomonas)
squamous cell lung cancer
tuberculosis
Wegener’s granulomatosis
pulmonary embolism
rheumatoid arthritis
aspergillosis, histoplasmosis, coccidioidomycosis
Causes of lung metastasis?
breast cancer
colorectal cancer
renal cell cancer
bladder cancer
prostate cancer
Causes of COPD?
Smoking
Alpha-1 antitrypsin deficiency
Then the C’s:
cadmium (used in smelting)
coal
cotton
cement
grain
Investigations for COPD?
post-bronchodilator spirometry to demonstrate airflow obstruction: FEV1/FVC ratio less than 70%
chest x-ray: hyperinflation, bullae, flat hemidiaphragm. Also important to exclude lung cancer
full blood count: exclude secondary polycythaemia
body mass index (BMI) calculation
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
How is a patient assessed for LTOT?
2 occasions at least 3 weeks apart in patients with stable COPD on optimal management.
Who should be offered LTOT?
pO2 of < 7.3 kPa
or
those with a pO2 of 7.3 - 8 kPa with:
- secondary polycythaemia
- peripheral oedema
- pulmonary hypertension
General management of COPD?
> smoking cessation advice
replacement therapy, varenicline or bupropion
annual influenza vaccination
one-off pneumococcal vaccination
pulmonary rehabilitation
Management COPD?
- a short-acting beta2-agonist (SABA) or short-acting muscarinic antagonist (SAMA) is first-line treatment
If this does not work:
2. Assess for asthmatic/steroid responsive features:
- higher blood eosinophil count
- recommend a full blood count for all patients as part of the work-up
- substantial variation in FEV1 over time (at least 400 ml)
- substantial diurnal variation in peak expiratory flow (at least 20%)
Management of COPD with non-asthmatic features?
- a short-acting beta2-agonist (SABA) or short-acting muscarinic antagonist (SAMA) is first-line treatment
- add a long-acting beta2-agonist (LABA) + long-acting muscarinic antagonist (LAMA)
if already taking a SAMA, discontinue and switch to a SABA
Management of COPD with asthmatic features?
- a short-acting beta2-agonist (SABA) or short-acting muscarinic antagonist (SAMA) is first-line treatment
- LABA + inhaled corticosteroid (ICS)
if patients remain breathless or have exacerbations offer triple therapy i.e. LAMA + LABA + ICS
if already taking a SAMA, discontinue and switch to a SABA
When should theophyllinebe considered?
recommends theophylline after trials of short and long-acting bronchodilators or to people who cannot used inhaled therapy
Who should be considered for prophylactic antibiotics in COPD?
patients should not smoke, have optimised standard treatments and continue to have exacerbations
Choice of prophylactic antibiotics in COPD?
Azithromycin
What should be checked before starting azithromycin?
ECG to exclude QT prolongation should also be done as azithromycin can prolong the QT interval
Features of cor pulmonale?
peripheral oedema, raised jugular venous pressure, systolic parasternal heave, loud P2
What is cryptogenic organising pneumonia?
Unknown aetiology
Affects distal bronchioles, respiratory bronchioles, alveolar ducts and alveolar walls
How does cryptogenic organising pneumonia present? Investigations?
cough, shortness of breath, fever and malaise.
Invx: Bloods show a leukocytosis and an elevated ESR and CRP
LFT’s may be restrictive, cholecystatic or normal
Imaging typically shows bilateral patchy or diffuse consolidative or ground glass opacities
How does cryptogenic organising pneumonia present? Investigations?
cough, shortness of breath, fever and malaise.
Invx: Bloods show a leukocytosis and an elevated ESR and CRP
LFT’s may be restrictive, cholecystatic or normal
Imaging typically shows bilateral patchy or diffuse consolidative or ground glass opacities
Genetics of cystic fibrosis?
Cystic fibrosis (CF) is an autosomal recessive disorder
defect in the cystic fibrosis transmembrane conductance regulator gene (CFTR), which codes a cAMP-regulated chloride channel
Where is the mutation in in CF?
Most common is delta F508 on the long arm of chromosome 7.
Organisms typically associated with infection in CF?
Staphylococcus aureus
Pseudomonas aeruginosa
Burkholderia cepacia*
Aspergillus
Features in 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
Management of cystic fiborsis?
- PT twice daily
- Lung transplant - chronic infection with Burkholderia cepacia is an important CF-specific contraindication to lung transplantation
CF should try to minimise contact with each other to prevent cross infection with Burkholderia cepacia complex and Pseudomonas aeruginosa
How to treat homozygous CF?
Lumacaftor/Ivacaftor (Orkambi)
-increases the number of CFTR proteins that are transported to the cell surface
ivacaftor is a potentiator of CFTR that is already at the cell surface
What is a contra-indication to lung transplant?
chronic infection with Burkholderia cepacia is an important CF-specific contraindication to lung transplantation
Mechanism of salbutamol?
- Short-acting inhaled bronchodilator. Relaxes bronchial smooth muscle through effects on beta 2 receptors
- Used in asthma and chronic obstructive pulmonary disease (COPD).
- Salmeterol has similar effects but is long-acting
Mechanism of ipratropium?
- Short-acting inhaled bronchodilator. Relaxes bronchial smooth muscle
- Used primarily in COPD
- Tiotropium has similar effects but is long-acting
What drug class is theophylline and what is its mechanism?
Methylxanthines
Non-specific inhibitor of phosphodiesterase resulting in an increase in cAMP
What is the new name of churg Strauss syndrome?
Eosinophilic granulomatosis with polyangiitis
What are the features of eosinophilic granulomatosis ?
asthma
blood eosinophilia (e.g. > 10%)
paranasal sinusitis
mononeuritis multiplex
pANCA positive in 60%
Differences between eosinophilic granulomatosis and granulomatosis with polyangitis?
what is idiopathic pulmonary fibrosis?
chronic lung condition characterised by progressive fibrosis of the interstitium of the lungs
What are the features of idiopathic pulmonary fibrosis?
progressive exertional dyspnoea
bibasal fine end-inspiratory crepitations on auscultation
dry cough
clubbing