respiratory 2 Flashcards
NIV - key indications?
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
type II respiratory failure secondary to chest wall deformity, neuromuscular disease or obstructive sleep apnoea
cardiogenic pulmonary oedema unresponsive to CPAP
weaning from tracheal intubation
Recommended intial setting for bi-level support in COPD?
Expiratory Positive Airway Pressure (EPAP): 4-5 cm H2O
Inspiratory Positive Airway Pressure (IPAP): RCP advocate 10 cm H20 whilst BTS suggest 12-15 cm H2O
back up rate: 15 breaths/min
back up inspiration:expiration ratio: 1:3
Asthma management algorithm?
Step 1 NICE
a low-dose inhaled corticosteroid (ICS)/formoterol combination inhaler to be taken as needed for symptom relief
this is termed anti-inflammatory reliever (AIR) therapy
if the patient presents highly symptomatic (for example, regular nocturnal waking) or with a severe exacerbation:
start treatment with low-dose MART (maintenance and reliever therapy, see below)
treat the acute symptoms as appropriate (e.g. a course of oral corticosteroids may be indicated)
Step 2 NICE
a low-dose MART
MART describes using an inhaled corticosteroid (ICS)/formoterol combination inhaler for daily maintenance therapy and the relief of symptoms as needed, i.e. regularly and as required
Step 3
a moderate-dose MART
Step 4
check the fractional exhaled nitric oxide (FeNO) level if available, and the blood eosinophil count NICE
if either of these is raised, refer to a specialist in asthma care
if neither FeNO nor eosinophil count is raised, consider a trial of either a leukotriene receptor antagonist (LTRA) or a long-acting muscarinic receptor antagonist (LAMA) used in addition to moderate-dose MART
if control has not improved, stop the LTRA or LAMA and start a trial of the alternative medicine (LTRA or LAMA)
Step 5
refer people to a specialist in asthma care when asthma is not controlled despite treatment with moderate-dose MART, and trials of an LTRA and a LAMA
What type of bacteria is Klebsiella?
Klebsiella pneumoniae is a Gram-negative rod that is part of the normal gut flora. It can cause a number of infections in humans including pneumonia (typically following aspiration) and urinary tract infections.
Features of Klebsiella?
more common in alcoholic and diabetics
may occur following aspiration
‘red-currant jelly’ sputum
often affects upper lobes
Prognosis in klebsiella pneumonia?
commonly causes lung abscess formation and empyema
mortality is 30-50%
Most common organisms isolated from patients with bronchiectasis:
Haemophilus influenzae (most common)
Pseudomonas aeruginosa
Klebsiella spp.
Streptococcus pneumoniae
What is Bronchiectasis?
Bronchiectasis describes a permanent dilatation of the airways secondary to chronic infection or inflammation.
How is bronchiectasis managed?
physical training (e.g. inspiratory muscle training) - has a good evidence base for patients with non-cystic fibrosis bronchiectasis
postural drainage
antibiotics for exacerbations + long-term rotating antibiotics in severe cases
bronchodilators in selected cases
immunisations
surgery in selected cases (e.g. Localised disease)
what causes CF?
In the UK 80% of CF cases are due to delta F508 on the long arm of chromosome 7. Cystic fibrosis affects 1 per 2500 births, and the carrier rate is c. 1 in 25
an autosomal recessive disorder causing increased viscosity of secretions (e.g. lungs and pancreas). It is due to a defect in the cystic fibrosis transmembrane conductance regulator gene (CFTR), which codes a cAMP-regulated chloride channel
What organisms may colonise CF patients?
Staphylococcus aureus
Pseudomonas aeruginosa
Burkholderia cepacia*
Aspergillus
what would be seen on spirometry on restrictive lung disease?
reduced FVC and normal or increased FEV1/FVC ratio
what is Bronchioitis obliterans?
Bronchiolitis obliterans (also known as obliterative bronchiolitis) is a rare complication of rheumatoid arthritis and is characterised by small airway inflammation and fibrosis, leading to airflow obstruction. This condition manifests as progressive dyspnoea and an obstructive spirometry pattern (reduced FEV1/FVC ratio)
progressive dyspnoea
obstructive pattern on spirometry
centrilobular nodules, bronchial wall thickening is seen on CT
What respiratory problems may be seen in patients with Rheumatoid arthritis?
pulmonary fibrosis
pleural effusion
pulmonary nodules
bronchiolitis obliterans
complications of drug therapy e.g. methotrexate pneumonitis
pleurisy
Caplan’s syndrome
Infection (possibly atypical) secondary to immunosupression
What are the thre main types of altitude related disorders?
There are three main types of altitude-related disorders: acute mountain sickness (AMS), which may progress to high altitude pulmonary oedema (HAPE) or high altitude cerebral oedema (HACE).
symptoms of acute montain sickness?
Acute mountain sickness is generally a self-limiting condition. Features of AMS start to occur above 2,500 - 3,000m, developing gradually over 6-12 hours and potentially last a number of days:
headache
nausea
fatigue
Prevention of acute moutnain sickness ?
the risk of AMS may actually be positively correlated to physical fitness
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
treatment: descent
What is High altitude pulmonary oedema ?
Happens above 4000m
HAPE
mechanism: hypobaric hypoxia → uneven hypoxic pulmonary vasoconstriction → uneven blood flow in the lungs → areas of the lung receiving more blood experience an increase in capillary pressure → more fluid leakage. Hypoxia may also directly increase capillary permeability, exacerbating fluid leakage into the alveolar space.
presents with classical pulmonary oedema features
what is the mechanism of altitude cerebral oedema?
in contrast to the HAPE, cerebral vasodilation is the problem. Hypoxia → cerebral vasodilation → elevated cerebral blood volume
also, hypoxia → increase in the permeability of the blood-brain barrier → capillaries in the brain more leaky → leading to fluid accumulation in the extracellular spaces
both these factors → cerebral oedema
presents with headache, ataxia, papilloedema
What is the management of HACE and HAPE
Management of HACE
descent
dexamethasone
Management of HAPE
descent
nifedipine, dexamethasone, acetazolamide, phosphodiesterase type V inhibitors*
oxygen if available
*the relative merits of these different treatments has only been studied in small trials. All seem to work by reducing systolic pulmonary artery pressure
First line investigations for asthma?
measure the eosinophil count OR fractional nitric oxide (FeNO)
diagnose asthma, without further investigations, if:
eosinophil is above the reference range
FeNO is ≥ 50 ppb
If asthma is not conformed by the eosinophil count ot FeNO what investigations can be done?
measure bronchodilator reversibility (BDR) with spirometry
diagnose asthma if:
the FEV1 increase is ≥ 12% and 200 ml or more from the pre-bronchodilator measurement, or
the FEV1 increase is ≥ 10% of the predicted normal FEV1
if spirometry is not available or it is delayed, measure peak expiratory flow (PEF) twice daily for 2 weeks
diagnose asthma if:
PEF variability (expressed as amplitude percentage mean) is ≥ 20%
If asthma is not confirmed by eosinophil count, FeNO, BDR or PEF variability but still suspected on clinical grounds:
refer for consideration of a bronchial challenge test
diagnose asthma if bronchial hyper-responsiveness is present
Investigations for asthma in children aged 5-16?
1st line - FeNO (diagnose asthma if FeNO is >35)
If the FeNO level is not raised, or if FeNO testing is not available:
measure bronchodilator reversibility (BDR) with spirometry
diagnose asthma if:
the FEV1 increase is ≥ 12% from the pre-bronchodilator measurement, or
the FEV1 increase is ≥ 10% of the predicted normal FEV1
if spirometry is not available or it is delayed, measure peak expiratory flow (PEF) twice daily for 2 weeks
diagnose asthma if:
PEF variability (expressed as amplitude percentage mean) is ≥ 20%
How do eosinophils play a direct role in airway inflammation?
eosinophils play a direct role in airway inflammation by releasing granules containing cytotoxic proteins like eosinophil peroxidase and major basic protein, which damage epithelial cells and perpetuate inflammation. Additionally, eosinophils are activated by interleukin-5 (IL-5) and other cytokines in the type 2 pathway, distinguishing them from neutrophils or lymphocytes
Why can Fractional exhaled nitric oxide (FeNO) be used to diagnose asthma?
Fractional exhaled nitric oxide (FeNO) reflects the level of nitric oxide produced by airway epithelial cells in response to eosinophilic inflammation, a hallmark of asthma. It is measured non-invasively by having the patient exhale steadily into a handheld device, which analyses nitric oxide concentration in parts per billion (ppb).
Obstructive lung disease vs restrictive lung disease on pulmonary function tests ?
causes of bilateral hilar lymphadenopathy?
The most common causes of bilateral hilar lymphadenopathy are sarcoidosis and tuberculosis.
Other causes include:
lymphoma/other malignancy
pneumoconiosis e.g. berylliosis
fungi e.g. histoplasmosis, coccidioidomycosis
Causes of pulmonary eosinophila?
Churg-Strauss syndrome
allergic bronchopulmonary aspergillosis (ABPA)
Loffler’s syndrome
eosinophilic pneumonia
hypereosinophilic syndrome
tropical pulmonary eosinophilia
drugs: nitrofurantoin, sulphonamides
less common: Wegener’s granulomatosis
Pulmonary eosinophilia describes a situation where there are increased numbers of eosinophils in the lung airways and parenchyma. This is generally associated with a blood eosinophilia.
What is Loffler’s syndrome?
transient CXR shadowing and blood eosinophilia
thought to be due to parasites such as Ascaris lumbricoides causing an alveolar reaction
presents with a fever, cough and night sweats which often last for less than 2 weeks.
generally a self-limiting disease
Is Extrinsic allergic alveolitis a pulmonary eosinophilia?
This condition, also known as hypersensitivity pneumonitis, is an immunologically mediated interstitial lung disease caused by repeated inhalation of a variety of antigens. The inflammatory response in extrinsic allergic alveolitis is primarily granulomatous and does not typically involve eosinophils
What is Alpha-1 antitrypsin (A1AT) deficiency?
A common inherited condition caused by a lack of a protease inhibitor normally produced by the liver
What is the primary role of A1AT?
To protect cells from enzymes such as neutrophil elastase
What condition is classically caused by A1AT deficiency in young, non-smoking patients?
Emphysema (chronic obstructive pulmonary disease)
On which chromosome is the A1AT gene located?
Chromosome 14
How is A1AT inherited?
In an autosomal recessive / co-dominant fashion
What liver conditions can occur in adults with A1AT deficiency?
- Cirrhosis
- Hepatocellular carcinoma
liver: cirrhosis and hepatocellular carcinoma in adults,
What investigations are used for A1AT deficiency?
- A1AT concentrations
- Spirometry: obstructive picture
What is a key management strategy for A1AT deficiency?
No smoking
Supportive measures
* Bronchodilators
* Physiotherapy
Intravenous alpha1-antitrypsin protein concentrates
Surgery - lung volume refuction surgery, lung transplant
What is Tidal Volume?
volume inspired or expired with each breath at rest
500ml in males, 350ml in females
What is inspitatory reserve volume?
maximum volume of air that can be inspired at the end of a normal tidal inspiration
inspiratory capacity = TV + IRV
Expiratory reserve volume?
maximum volume of air that can be expired at the end of a normal tidal expiration
significantly reduced in obesity (increased abdominal fat mass pushes up against the diaphragm, reducing the volume of air that can be expelled)
What is residual volume?
volume of air remaining after maximal expiration
increases with age
RV = FRC - ERV
What is functional residual capacity ?
the volume in the lungs at the end-expiratory position
FRC = ERV + RV
What is vital capacity?
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 the total lung capacity?
Total lung capacity (TLC) is the sum of the vital capacity + residual volume
What is the physiological dead space?
VD = tidal volume * (PaCO2 - PeCO2) / PaCO2
where PeCO2 = expired air CO
What is Psitacosis?
Psittacosis is infection caused by Chlamydia psittaci.
Chlamydia psittaci is an obligate intracellular bacteriu
ransmission is typically from birds or bird secretions including urine and faeces, typically occurring after cleaning bird cages
Features of Psittacosis?
sittacosis should be suspected in a combination of typical fever with a history of bird contact (reported in 84%) or a presentation with pneumonia and severe headache or organomegaly and failure to respond to penicillin-based antibiotics.
Patients typically present with a subacute onset of:
Flu-like symptoms (90%): fever, headache and myalgia
Respiratory symptoms (82%): dyspnoea, dry cough and chest pain
Signs:
Chest: unilateral crepitations and vesicular breathing (common), evidence of pleural effusion (uncommon)
Abdomen: hepatomegaly and splenomegaly (rare)
Tratment for Psittacosis?
1st-line: tetracyclines e.g. doxycycline
2nd-line: macrolides e.g. erythromycin
Why does pulmonary haemorrhage lead to increased TLCO?
In pulmonary haemorrhage, there is extravasation of blood into the alveolar spaces. This increases the amount of haemoglobin available in the alveoli for carbon monoxide binding, leading to an increased TLCO measurement. The presence of additional red blood cells in the alveolar space enhances the gas transfer capacity, as carbon monoxide has a high affinity for haemoglobin.
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
What is allergic broncopulmonary aspergillosis
Allergic bronchopulmonary aspergillosis results from an allergy to Aspergillus spores. In the exam questions often give a history of bronchiectasis and eosinophilia.
Features of allergic broncopulmonary aspergillosis ?
bronchoconstriction: wheeze, cough, dyspnoea. Patients may have a previous label of asthma
bronchiectasis (proximal)
diagnosis of allergic broncopulmonary aspergillosis ?
eosinophilia
flitting CXR changes
positive radioallergosorbent (RAST) test to Aspergillus
positive IgG precipitins (not as positive as in aspergilloma)
raised IgE
Major criteria for the diagnosis are:
Clinical features of asthma
Proximal bronchiectasis
Blood eosinophilia
Immediate skin reactivity to Aspergillus antigen
Increased serum IgE (>1000 IU/ml)
Minor criteria:
Fungal elements in sputum
Brown flecks in sputum
Delayed skin reactivity to fungal antigens
Management of allergic bronocpulmonary aspergillosis?
oral glucocorticoids
itraconazole is sometimes introduced as a second-line agent
what is silicosis?
Silicosis is a fibrosing lung disease caused by the inhalation of fine particles of crystalline silicon dioxide (silica). It is a risk factor for developing tuberculosis (silica is toxic to macrophages).
Occupations at risk of silicosis
mining
slate works
foundries
potteries
Features of Silicosis?
upper zone fibrosing lung disease
‘egg-shell’ calcification of the hilar lymph nodes
What is Atelectasis?
Atelectasis is a common postoperative complication in which basal alveolar collapse can lead to respiratory difficulty. It is caused when airways become obstructed by bronchial secretions.
What are the features of Atelectasis?
it should be suspected in the presentation of dyspnoea and hypoxaemia around 72 hours postoperatively
What is the management of atelectasis?
positioning the patient upright
chest physiotherapy: breathing exercises
Paraneoplastic features of lung cancer?
Small cell
squamous cell
adenocarcinoma
**Small cell
**ADH
ACTH - not typical, hypertension, hyperglycaemia, hypokalaemia, alkalosis and muscle weakness are more common than buffalo hump etc
Lambert-Eaton syndrome
**Squamous cell
**parathyroid hormone-related protein (PTH-rp) secretion causing hypercalcaemia
clubbing
hypertrophic pulmonary osteoarthropathy (HPOA)
hyperthyroidism due to ectopic TSH
**Adenocarcinoma
**gynaecomastia
hypertrophic pulmonary osteoarthropathy (HPOA)
what may lead to respiratory alkalosis?
anxiety leading to hyperventilation
pulmonary embolism
salicylate poisoning*
CNS disorders: stroke, subarachnoid haemorrhage, encephalitis
altitude
pregnancy
Contraindications to surgical resection 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
presenting 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
Other features of cystic fibrosis
short stature
diabetes mellitus
delayed puberty
rectal prolapse (due to bulky stools)
nasal polyps
male infertility, female subfertility
What is the mechanism of action of Leukotriene receptor antagonists?
a class of drugs that block the action of leukotrienes, inflammatory mediators derived from arachidonic acid via the 5-lipoxygenase pathway.
LTRAs, such as montelukast and zafirlukast, competitively block the CysLT1 receptor found in the airways, thereby reducing the effects of leukotrienes.
Leukotrienes contribute to the pathophysiology of asthma by promoting bronchoconstriction, airway hyperresponsiveness, mucus secretion, and eosinophilic inflammation.
What effect for LTRA have?
Decreased bronchoconstriction
Reduced mucus production
Attenuation of airway inflammation
Improved airway calibre and reduced symptoms of asthma
Adverse effects of LTRA?
neuropsychiatric effects associated with montelukast, including agitation, sleep disturbances, depression, and, rarely, suicidal ideation. Patients should be monitored for these symptoms, and the drug should be discontinued if they occur.
Hepatic dysfunction: Zafirlukast has been associated with hepatic impairment, and liver function should be monitored during therapy.
Churg-Strauss syndrome: As mentioned, caution is advised when tapering corticosteroids in patients starting LTRAs, as CSS may be unmasked.
COPD severity staging?
The severity of COPD is categorised using the FEV1*:
*note that the grading system has changed following the 2010 NICE guidelines. 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
High risk characteristics indicating insertion of chest darin in pneumothroax?
haemodynamic compromise (suggesting a tension pneumothorax)
significant hypoxia
bilateral pneumothorax
underlying lung disease
≥ 50 years of age with significant smoking history
haemothorax
What is Eosinophilic granulomatosis with polyangiitis (EGPA)?
Eosinophilic granulomatosis with polyangiitis (EGPA) is now the preferred term for Churg-Strauss syndrome. It is an ANCA associated small-medium vessel vasculitis.
What are the features of Eosinophilic granulomatosis with polyangiitis (EGPA)?
asthma
blood eosinophilia (e.g. > 10%)
paranasal sinusitis
mononeuritis multiplex
renal involvement occurs in around 20%
pANCA positive in 60%
What may precipitate Eosinophilic granulomatosis with polyangiitis?
Leukotriene receptor antagonists may precipitate the disease.
Causes of pulmonary fibrosis predominately affecting the upper zones?
hypersensitivity pneumonitis (also known as extrinsic allergic alveolitis)
coal worker’s pneumoconiosis/progressive massive fibrosis
silicosis
sarcoidosis
ankylosing spondylitis (rare)
histiocytosis
tuberculosis
radiation-induced pulmonary fibrosis
may develop following radiotherapy for breast or lung cancer
typically seen between 6 and 12 months following completion of radiotherapy course
Acronym for causes of upper zone fibrosis:
CHARTS
C - Coal worker’s pneumoconiosis
H - Histiocytosis/ hypersensitivity pneumonitis
A - Ankylosing spondylitis
R - Radiation
T - Tuberculosis
S - Silicosis/sarcoidosis
Causes of fibrosis predominately affecting the lower zones?
idiopathic pulmonary fibrosis
most connective tissue disorders (except ankylosing spondylitis) e.g. SLE
drug-induced: amiodarone, bleomycin, methotrexate
asbestosis
What is Extrinsic allegic alveolitis?
Extrinsic allergic alveolitis (EAA, also known as hypersensitivity pneumonitis) is a condition caused by hypersensitivity induced lung damage due to a variety of inhaled organic particles.
What type of hypersensitivity reactions occure in extrinsic allergic alveolitis?
It is thought to be largely caused by immune-complex mediated tissue damage (type III hypersensitivity) although delayed hypersensitivity (type IV) is also thought to play a role in EAA, especially in the chronic phase.
Examples of extrinsic allergic alveolitis?
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*
How does extrinsic allergic alveolitis present?
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
Investigations and management for Extrinsic allergic alveolitis?
Investigation
imaging: upper/mid-zone fibrosis
bronchoalveolar lavage: lymphocytosis
serologic assays for specific IgG antibodies
blood: NO eosinophilia
Management
avoid precipitating factors
oral glucocorticoids
Paraneoplastic features of lung cancer?
Paraneoplastic features of lung cancer
squamous cell: PTHrp, clubbing, HPOA
small cell: ADH, ACTH, Lambert-Eaton syndrome
what type of lung cancer is PTH related peptide secretion seen in?
Squamous cell lung cancer
What is a contraindication to lung transplantation in cystic fibrosis?
chronic infection with Burkholderia cepacia is an important CF-specific contraindication to lung transplantation
Chronic infection with Burkholderia cepacia is an important CF-specific contraindication to lung transplantation. Patients with Burkholderia cepacia complex, particularly the Burkholderia cenocepacia species, have an increased risk of mortality due to recurrent disease after transplantation. Burkholderia cepacia typically causes a more rapid progression of disease associated with a deterioration in lung function and FEV1. It is also responsible for an often fatal necrotizing pneumonia known as the ‘cepacia syndrome.’
How many hours a day should COPD patients with LTOT wear their oxygen ?
15 hours
When should LTOT be given to patients with COPD?
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 are the features of cor pulmonale?
features include peripheral oedema, raised jugular venous pressure, systolic parasternal heave, loud P2
Normal genes seen for alpha 1 antitripsin and what is seen in defiency?
normal: PiMM
heterozygous: PiMZ
evidence base is conflicting re: risk of emphsema
however, if non-smoker low risk of developing emphsema but may pass on A1AT gene to children
homozygous PiSS: 50% normal A1AT levels
homozygous PiZZ: 10% normal A1AT levels
Staging of sarcoidosis on CXR?
A chest x-ray may show the following changes:
stage 0 = normal
stage 1 = bilateral hilar lymphadenopathy (BHL)
stage 2 = BHL + interstitial infiltrates
stage 3 = diffuse interstitial infiltrates only
stage 4 = diffuse fibrosis
What bacteria is responsible for malt workers lung?
Aspergillus clavatus causes malt workers’ lung, a type of EAA
what is responsible for bird fanciers’ lung?
avian proteins from bird droppings
What is responsible for farmers lung?
spores of Saccharopolyspora rectivirgula from wet hay (formerly Micropolyspora faeni)
features of eosinophilc granulomatosis with polyangitis?
Features
asthma
blood eosinophilia (e.g. > 10%)
paranasal sinusitis
mononeuritis multiplex
renal involvement occurs in around 20%
pANCA positive in 60%
Granulomatosis with polyangitis (wegener’s) vs eosinophilic granulomatosis with polyangitis (churg strauss)
Pre-disposing factors to OSA?
Predisposing factors
obesity
macroglossia: acromegaly, hypothyroidism, amyloidosis
large tonsils
Marfan’s syndrome
Diagnostic tests for obstructive 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 OSA?
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 Varenicline?
When should it be started
What is the course length
Saide effects
Contraindications
a nicotinic receptor partial agonist
should be started 1 week before the patients target date to stop
the recommended course of treatment is 12 weeks (but patients should be monitored regularly and treatment only continued if not smoking)
has been shown in studies to be more effective than bupropion
nausea is the most common adverse effect. Other common problems include headache, insomnia, abnormal dreams
varenicline should be used with caution in patients with a history of depression or self-harm. There are ongoing studies looking at the risk of suicidal behaviour in patients taking varenicline
contraindicated in pregnancy and breastfeeding
How should secondaru spontanous pneumothorax be managed?
Patients with a secondary spontaneous pneumothorax that is managed conservatively should be monitored as an inpatient
What is Bupropion?
When should it be started
Side effects and contraindicaitons ?
a norepinephrine-dopamine reuptake inhibitor and nicotinic antagonist
unlike many antidepressants it has a minimal effect on serotonin
should be started 1 to 2 weeks before the patient’s target date to stop
small risk of seizures (1 in 1,000)
contraindicated in epilepsy, pregnancy and breast feeding. Having an eating disorder is a relative contraindication
What is idiopathic pulmonary fibrosis?
Idiopathic pulmonary fibrosis (IPF, previously termed cryptogenic fibrosing alveolitis) is a chronic lung condition characterised by progressive fibrosis of the interstitium of the lungs. Whilst there are many causes of lung fibrosis (e.g. medications, connective tissue disease, asbestos) the term IPF is reserved when no underlying cause exists.
In what age group is idopathic pulmonary fibrosis seen ?
50-70 years and is twice as common in men.
What are the features of idiopathic pulmonary fibrosis?
progressive exertional dyspnoea
bibasal fine end-inspiratory crepitations on auscultation
dry cough
clubbing
How is idiopathic pulmonary fibrosis diagnosed?
spirometry: classically a restrictive picture (FEV1 normal/decreased, FVC decreased, FEV1/FVC increased)
impaired gas exchange: reduced transfer factor (TLCO)
imaging: 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
ANA positive in 30%, rheumatoid factor positive in 10% but this does not necessarily mean that the fibrosis is secondary to a connective tissue disease. Titres are usually low
How is idiopathic pulmonary fibrosis managed ?
Management
pulmonary rehabilitation
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 (see NICE guidelines)
many patients will require supplementary oxygen and eventually a lung transplant
Prognosis
poor, average life expectancy is around 3-4 years
What is Kartagener’s syndrome?
Kartagener’s syndrome (also known as primary ciliary dyskinesia) was first described in 1933 and most frequently occurs in examinations due to its association with dextrocardia (e.g. ‘quiet heart sounds’, ‘small volume complexes in lateral leads’)
Pathogenesis
dynein arm defect results in immotile cilia
Features of Kartagener’s syndrome?
Features
dextrocardia or complete situs inversus
bronchiectasis
recurrent sinusitis
subfertility (secondary to diminished sperm motility and defective ciliary action in the fallopian tubes)
when is calcificaion in lung mets seen ?
Calcification in lung metastases is uncommon except in the case of chondrosarcoma or osteosarcoma.
What is the bronchial challenge test?
The bronchial challenge test assesses airway hyperresponsiveness, a characteristic feature of asthma, by measuring the airway’s response to a provocative agent such as methacholine or histamine. In asthma, heightened bronchial smooth muscle reactivity and inflammation lead to excessive narrowing of the airways when exposed to these agents, resulting in a significant decline in FEV1
If asthma is not confirmed by eosinophil count, FeNO, BDR or PEF variability but still suspected then refer for consideration of….
bronchial challenge test
What is ARDS?
Acute respiratory distress syndrome (ARDS) is caused by the increased permeability of alveolar capillaries leading to fluid accumulation in the alveoli, i.e. non-cardiogenic pulmonary oedema. It is a serious condition that has a mortality of around 40% and is associated with significant morbidity in those who survive.
Causes of acute respiratory distress syndrome?
infection: sepsis, pneumonia
massive blood transfusion
trauma
smoke inhalation
acute pancreatitis
Covid-19
cardio-pulmonary bypass
Clinical features?
dyspnoea
elevated respiratory rate
bilateral lung crackles
low oxygen saturations
Diagnosis of ARDS?
A chest x-ray and arterial blood gases are the key investigations.
Criteria (American-European Consensus Conference)
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)
Management of ARDS?
due to the severity of the condition patients are generally managed in ITU
oxygenation/ventilation to treat the hypoxaemia
general organ support e.g. vasopressors as needed
treatment of the underlying cause e.g. antibiotics for sepsis
certain strategies such as prone positioning and muscle relaxation have been shown to improve outcome in ARDS
what is the normal vital capacity ?
4,500ml in males, 3,500 mls in females
CURB 65
Management of CAP?
Management of low-severity community acquired pneumonia
amoxicillin is first-line
if penicillin allergic then use a macrolide or tetracycline
NICE now recommend a 5 day course of antibiotics for patients with low severity community acquired pneumonia
Management of moderate and high-severity community acquired pneumonia
dual antibiotic therapy is recommended with amoxicillin and a macrolide
a 7-10 day course is recommended
NICE recommend considering a beta-lactamase stable penicillin such as co-amoxiclav, ceftriaxone or piperacillin with tazobactam and a macrolide in high-severity community acquired pneumonia
Discharge criteria and advice post-discharge
CAP
NICE recommend that patients are not routinely discharged if in the past 24 hours they have had 2 or more of the following findings:
temperature higher than 37.5°C
respiratory rate 24 breaths per minute or more
heart rate over 100 beats per minute
systolic blood pressure 90 mmHg or less
oxygen saturation under 90% on room air
abnormal mental status
inability to eat without assistance.
what is seen on spirometry of an obese patient?
. A reduced FEV1 and FVC with a normal FEV1/FVC ratio, and reduced expiratory reserve volume may be observed in cases of obesity
COPD causes?
Smoking!
Alpha-1 antitrypsin deficiency
Other causes
cadmium (used in smelting)
coal
cotton
cement
grain
What is Kartagener’s syndrome
Kartagener’s syndrome (also known as primary ciliary dyskinesia) was first described in 1933 and most frequently occurs in examinations due to its association with dextrocardia (e.g. ‘quiet heart sounds’, ‘small volume complexes in lateral leads’)
Pathogenesis
dynein arm defect results in immotile cilia
Features of Kartagener’s syndrome?
Features
dextrocardia or complete situs inversus
bronchiectasis
recurrent sinusitis
subfertility (secondary to diminished sperm motility and defective ciliary action in the fallopian tubes)
