Resp Flashcards
When has or is the peak of asbestos-related diseases due or did present?
Over the 5-10 years (I.e., around 2019-2024), due to the long latent period between asbestos exposure and disease.Asbestos use was banned in the 1980’s but many people worked with it up until then.
What nations still produce and use lots of asbestos?
Brazil, Russia, China, Kazakhstan. So important to know about asbestos related disease not only for the point of view of uk workers who used to work with it, but migrants from countries that still use it.
What are the two types of asbestos? How widely used are/were they?
White - chrysotile, accounts for more than 95% of use worldwide! serpentine minerals! curly long woven fibres.Blue/brown - corcoidolite, amosite, and others - straighter, brittle, less malleable.
What are the useful properties of asbestos which meant it was and still is used so widely?
Heat, fire, and chemical resistance.Electrical and sound insulation.Medium tensile strength.Therefore very valuable in industry, especially in building and construction.
What are the four grades of asbestos-related lung disease?
1) benign disease (pleural plaques, diffuse pleural thickening, benign pleural effusion).2) asbestososis (a type of interstitial lung disease).3) lung cancer.4) malignant mesothelioma (cancer of the pleural layer, very dangerous).
What is the epidemiology of asbestos-related disease? (Three points)
As mentioned previously, peak onset between now and 2024.Male:female ratio of 4:1 (due to exposure; more men worked with asbestos than women).It is rare under the age of 40 (due to long latent period).
What is the pathophysiology of asbestos related disease? What properties of asbestos molecules make it difficult for the lungs to clear? (Name 3).
The fibres become airborne, are inhaled, and are trapped inside the lungs. They are classified as carcinogens. Mucocilliary clearance gets rid of some, but not all of these fibres, because of their special properties:1) they are long, therefore cannot be completely enclosed by macrophages, and are not effectively cleared.2) they are thin - this mean they can travel deep into the respiratory network, beyond they point where mucucilliary clearance occurs.3) biopersistance - they are not broken down, they accumulate over time.
What are the risk factors for developing asbestos related disease? (name 3).
1) the dose of asbestos that an individual is exposed to; the quantity and duration of that exposure.2) type and size of fibre; it is thought that blue or brown asbestos (amphibole sub types) has a greater propensity for causing mesothelioma than the white (chrysotile). This is due to the structure of the molecule.3) personal factors: smoking, pre-existing lung disease, sex, age, etc.
Is smoking a risk factor for developing mesothelioma?
A sneaky question!Smoking on it’s own is NOT a risk factor for developing mesothelioma.BUT if you are exposed to asbestos AND you are a smoker, you have around twice the risk of developing mesothelioma. Also this population has 50-90% increased risk of developing asbestos-related lung cancer.Weird, huh?
Apart from people who directly handle asbestos, who else is at risk of asbestos exposure. (Name two).
The families of the people exposed - they are exposed to, e.g., asbestos on the clothes of the worker.Also people who live close to sites where asbestos is manufactured, or where asbestos-containing products are manufactured.
What occupation carries the greatest risk of asbestos exposure?
Mining asbestos!Fortunately, the UK never had asbestos mines…but other countries did (and do) and migration means we may see the results of this.
What occupations are at-risk for asbestos exposure? (There are seven named here; name 4).
1) miner of asbestos (not in the uk).
2) shipyard workers. (E.g., insulation of boiler pipes, incinerators, pipes. Fibres build up in poorly ventilated areas of the ship).
3) demolition. (Disturbed fibres become airborne).
4) car manufacturing. (Manufacture or repair of breaks and clutch pads)
5) construction. (Electricians, cement production, insulators, pipe-fitters, steel workers, plumbers, roofers, welders).
6) railway workers. (Especially those involved in carriage insulation).
7) manufacturing. (Specifically manufacturing of asbestos containing products for home and industry).
Ini addiction to occupational exposure, and the families of these workers, and the people who live near sites of asbestos manufacture, who else might be exposed?
Anyone who tampers with products that contain asbestos!Any building built prior to 1980 probably has asbestos in it - which is ok as long as it is not disturbed.Self employed plumbers, electricians, builders and carpenters of today may unwittingly expose themselves.Also, DIY enthusiasts may do the same.
Who should remove asbestos?
By a licensed contractor, as set out by the UK’s HSE. But this is NOT often done!
Who should a GP be most suspicious of asbestos related disease in? What should they do?
Middle aged or elderly men, with a history of asbestos exposure, presenting with respiratory symptoms, especially SOBOE.GP’s should: take a thorough occupational and social history, clinical history, full exposure to asbestos history (if known, the type of asbestos exposed to, and the duration of that exposure), full clinical examination.
According to the 2005 NICE guidelines, what should be done with a patient who has a history of asbestos exposure, presenting with SOB, chest pain, unexplained systemic symptoms, or clinical suspicion of cancer?
They should be referred urgently (2WW) to the lung physicians!Duh!
Other than an CXR which can be order in primary care, what secondary care investigations might be useful if asbestos related disease is suspected?
Lung function testing.High resolution CT scan (v sensitive for detecting early fibrosis and pleural plaques).
Who should you tell to stop smoking?
Everybody, of course!But anyone with a history of asbestos exposure should be told twice, because they have double the risk of lung cancer and mesothelioma.
Who should be offered the annual influenza and pneumococcal vaccinations?
Those who have been diagnosed with asbestososis, mesothelioma, or lung cancer.
COPD patients.
What might be the clinical presentation of someone with benign asbestos related disease?
SOB, chest pain.CXR would show pleural plaques (usually asymptomatic) and diffuse pleural thickening.
What might be the presenting symptoms of asbestososis?
SOBOE, dry cough; later, finger clubbing, cor pulmonale.
What might be the presenting features of asbestos related lung cancer?
Usually none at first! Occasional dry cough.Advanced stage: haemoptysis, cough, loss of weight, chest pain, fatigue, SOB, pleural effusion.
What might be the presenting symptoms of mesothelioma?
Usually none at first; sometimes some chest pain and SOB.Advanced disease: SOB, severe and progressive chest pain, pleuritic chest pain, constitutional symptoms such as loss of weight and fatigue.
What is the most common response to exposure to asbestos? What is the latent period? What does this pathology represent? What symptoms might thee patients have, what is there prognosis, and how should they be treated?
Pleural plaques, which usually occur 20-40 years after exposure.They are usually asymptomatic. They are areas of fibrous thinking that usually become calcified over time, usually affecting the parietal pleura (occasionally the visceral pleura affected too).They do not generally progress to anything nasty - they are benign - and it is important to tell patients this; the treatment is reassurance and monitoring in primary care.However, it would be prudent to advise these patients to report any red flag signs, e.g., haemoptysis, persistent chest pain, or SOB should they develop.
What is asbestos related diffuse pleural thickening?
This refers to fibrosis of the visceral pleura as well as loss of pleural space.On a CXR, usually appears as unilateral or bilateral diffuse pleural thickening, with blunting of costophrenic angles.
What often precedes the development of diffuse pleural thickening (DPT) and can facilitate disease progression?
Benign asbestos related pleural effusion.
What do benign asbestos related pleural effusion and benign diffuse pleural thickening have in common?
They are both diseases of exclusion - other causes must be ruled out first, e.g., TB, malignancy; or mesothelioma in the case of pleural thickening.Some patients with a benign asbestos related pleural effusion will need a pleuritic tap if it is large or symptomatic.
When doe benign asbestos related pleural effusion present? What type of effusions are they?
The lag time is short compared to other forms of asbestos related disease - as short as ten years.They are often small exudative effusions, and may regress spontaneously.They may also herald the onset of benign diffuse pleural thickening.
What investigations are required if benign asbestos-related diffuse pleural thickening is suspected?
Intitially, HRCT is the imagining of choice - it is more sensitive than CXR at assessing DPT and it’s extent.However, as asbestos related DPT is a diagnosis of exclusion, other investigations are then usually performed, possibly including MRI, positron omission tomography, and pleural biopsy (to exclude malignant mesothelioma).
Diffuse pleural thickening (DPT) has many causes other than asbestos exposure, hence asbestos related DPT being a diagnosis of exlusion.What can cause DPT? (Name 5)
1) asbestos exposure2) previous thoracotomy or pleurodesis3) TB4) bacterial infection5) connective tissue disease6) haemothorax
What would be the spirometry of someone with diffuse pleural thickening?
A restrictive ventilators defect.
What treatment is there for diffuse pleural thickening?
Not much - it is generally just supportive. Occasionally, non-invasive ventilation is used when type 2 respiratory failure develops.
What is the definition of asbestososis? What is it the most common of?
Bilateral pulmonary fibrosis secondary to asbestos inhalation. Usually there is a lag time of at least 20 years.It is the most common of all the pneumoconiosis diseases and has similar characteristics to interstitial lung fibrosis.
What is the pathogenesis of asbestososis?
Asbestos is fibrogenic to the lungs. Asbestos deposits in the lung causes collagen deposits in the alveolar epithelium and surrounding tissues.
What is the most common presenting feature of asbestosis?
SOBOE and non productive cough.Advanced features include chest tightness and features related to pulmonary hypertension and cor pulmonale.
What examination findings might there be to be found on someone with asbestososis?
Two thirds of patients have fine bi-basal end-inspiritory crackles.Finger clubbing and reduced chest expansion may also be seen.Note that radiographic or pulmonary function testing suggestive of interstitial lung disease often precedes the development of clinical signs.
As with all forms of interstitial fibrosis, what will be found on lung function testing in asbestososis? How about chest radiography/HRCT findings? And pulse oximetry? If this isn’t sufficient for a diagnosis, what can be done, and what would be seen?
Lung function testing would show restrictive pattern with reduction in total lung capacity, vital capacity, and small airway flow rates.CXR will show reticulonodular shadowing in the lower zones.HRCT will show interstitial infiltrates.Pulse oximetry may give evidence of desaturation on exertion.If this is not enough, or if diagnosis is in doubt, then a tissue sample can be taken - pathology will show fibrosis and presence of ferringous bodies (asbestos fibres with a ferritin coating) in the interstitium.
What are the treatment options for asbestososis?
Unfortunately, asbestososis does not respond to convention treatments for interstitial lung diseases - so no role for steroids or immunosuppressants.So management is initially generally supportive.Supplementary oxygen should be offered for those with those at rest or on exercise.Respiratory physiotherapy also plays an important role, as does palliation in the latter stages.
What type of lung cancer does asbestos exposure increase the risk of?
All types!Though note (again!) that smoking + asbestos exposure increases the risk more than would be expected - about twice as much!Asbestos related small cell and non-small cell lung cancers are clinically identical to other tumours of these types.
Where does mesothelioma arise?
Typically in the pulmonary pleura (80%).BUT can also occur peritoneum, the pericardium, and even the tunica vaginalis of the testes!It develops from the mesothelial cells found in these places.
Mesothelioma usually arises secondary to asbestos exposure, with an average lag time of 32 years. But what else can cause it?
Exposure to other fibrous silicate materials, e.g., erionite. Irradiation. Smoking does not (unless also exposed to asbestos - in which case the risk is doubled!)
What are the typical presenting symptoms of malignant mesothelioma?
Dyspnoea (often secondary to pleural effusion or pleural thickening).Chest pain (often described as progressive and dull).Systemic features such as weight loss and fatigue.If peritoneal mesothelioma, then may get abdominal pain, ascites, or features of bowel obstruction.
Does mesothelioma typically metastasise? If so where to?
No, it is not common to.But when it does, typical sites include bone, liver, and lymphatics.
What radiographical features might alert you to the possibility of mesothelioma in a patient with a history of asbestos exposure?What is required to confirm the diagnosis? How is this done?
Pleural thickenings, chest wall masses, or effusion notes on CXR or HRCT.The diagnosis is confirmed by histological and/or cytological examination (important if money / reparations is an issue!!).Pleural aspiration or US-guided pleural biopsy are the usual methods of obtaining a sample; if the facilities exist, then thoracoscopy can be employed to drain the pleural fluid, get a biopsy of the pleura, and also carry out a pleurodesis.
What system is used to stage malignant mesothelioma?
TNM staging.
What is the prognosis of malignant mesothelioma?
Extremely poor. Even with treatment, life expectancy is 8-14 months from time of diagnosis. Partly this is due to late presentation.
What are the treatments used for mesothelioma?
Chemotherapy, radiotherapy, or surgery (pneumonectomy).But these are usually palliative measures, and do little to improve survival times.Treatment is therefore often symptomatic and palliative.
Does asbestos exposure ever result on disease in extra-pulmonary sites?
There is some evidence that it can cause peritoneal mesothelioma, autoimmune disease, and reproductive malignancies (ovarian cancer and testicular malignant mesothelioma).The hypothesis is that swallowing fibres of e.g., chrysotile from occupational exposure or swallowing water from pipes lined with asbestos can lead to this. But all studies involved in this have been small and low-powered.
In what part of the country do most asbestos support groups reside and why?
The north of England and Scotland as this is where asbestos use was highest.
In general, what is the role of the GP in supporting a patient diagnosed with an asbestos-related condition?
To give information on the nature of the disease and the extent of lung damage.To give an idea of prognosis.To sometimes give treatment (though this is often secondary care).Guidance on financial compensation.Sign posting the patient to appropriate support- e.g., assessment in a dedicated occupational respiratory clinic by OH physicians working with respiratory physicians.
Is there a single website that lists all the mesothelioma support groups?
Mesothelioma UK.Provides details of all support groups in the UK.Also lots of specialist mesothelioma information.
What compensations exist in the UK for those affected by asbestos related disease? (5 facts, name 4).
-Since 2007, those in England and Wales cannot claim for benign pleural plaques.-IIDB : weekly allowance payed by department of work and pensions to those who contracted an industrial disease during their employment.-The pneumoconiosis etc (workers compensation) act 1979: a lump sum payment payable to those who cannot claim from former employers because those employers are no longer trading. Can be claimed by dependants after death of patient.-Diffuse Mesothelioma Payment: since 2008, lump sum payable to those diagnosed with mesothelioma; may be claimed by dependants of the dead.-A War Disablement Pension: may be claimed if disease arises from exposure during service in the armed forces in the UK.
What percentage of adults in the UK smoke?
About 20%! And that has stayed stable for the last 5 years.
How much % of the adult population in the UK is affected by COPD?
About 6%, though many remain undiagnosed.It is estimated that COPD will become the worlds 3rd largest cause of death by 2020.
Very broadly, how is the multidisciplinary management of COPD divided? (Name 3, there are 4).
1) smoking ceasation.2) pulmonary rehabilitation.3) other multidisciplinary interventions.4) medical management including including inhaled and oral pharmacotherapies and oxygen therapy.
When is management of COPD seen as being successful?
If there is a reduction in exacerbations of the disease.
What is the most beneficial management step for COPD patient? What evidence? How can this be achieved?
Stopping smoking. After 5 years, rate of FEV1 decline and related symptom frequency was significantly reduced in patients who stopped smoking.Options include self help materials, quit lines (e.g., NHS stop smoking sevice), group behavioural counselling, brief interventions by healthcare professionals working at the GP practice, and pharmacotherapies.
What pharmacological therapies exist to help quit smoking? Should they be used together? What should be done before/when starting them?
Current pharmacotherapies include nicotine replacement therapy, varenicline, and bupropion.They should not be used together.Choice of pharmacotherapy should be discussed with patient, previous ones used, interactions should be discussed.A quit date should be agreed on and pharmacotherapy started on the same day. Pharmacotherapies are best used when used in combination with behavioural therapies.
Describe the transtheoretocal model of health behaviour change? (As used in e.g., quitting smoking and addiction?)
Addiction –> pre-contemplation –> contemplation –> preparation Preparation can either lead to action or relapse.Relapse –> addiction.Action can either lead to maintenance or relapse.Maintenance seems to lead to relapse, but it seems to me that it might result in itself - maintenance of non-addiction.
What is the system adopted by NICE used to grade treatment of COPD?
GOLD grading system/criteria. Grades disease severity and guides management. Invented by the Global Initiative for Chronic Obstructive Lung Disease (GOLD).
What does the GOLD criteria for COPD measure to grade which stage of disease progression has been reached? (3 things).
1) FEV1/FVC.2) FEV1%3) Subjective and objective patient experience - essentially dyspnoea, number of exacerbations, exercise tolerance.
How many stages of GOLD are there? What are they known as? What defines them?
There are 4 stages:1) mild COPD: FEV1/FVC less than 70%; FEV1 equal to or greater than 80% predicted; no or minimal symptoms.2) moderate COPD: FEV1/FVC less than 70%; FEV1 50-79% predicted; mild symptoms (e.g., dyspnoea on significant exertion)3) severe COPD: FEV1/FVC less than 70%; FEV1 30-49% predicted; increasing symptoms (e.g., recurrent exacerbations, poor exercise tolerance).4) very severe COPD: FEV1/FVC less than 70%; FEV1 less than 30% predicted or less than 50% plus respiratory failure; serve symptoms, e.g., minimal exercise tolerance, dyspnoea at rest.
What medical treatment should be used at GOLD stage 1 for COPD? What would indicate progression to stage two is possible?
SABA or SAMA to be used for symptom relief. If used more than 4 times a day, regular exacerbations, or continued symptoms, then consider going to stage 2.
What medical treatment should be used at GOLD stage 2 for COPD? What would indicate progression to stage three is possible?
Addition of LAMA or LABA. Continue SABA or SAMA.If continued symptoms such as breathlessness or recurrent exacerbations then consider stage three.
What medical treatment should be used at GOLD stage 3 for COPD? What would indicate progression to stage four is possible?
Continue LAMA; consider inhaled corticosteroid and/or LABA combined inhaler.If continued symptoms such as breathlessness or recurrent exacerbations then consider stage four.
What medical treatment should be used at GOLD stage 4 for COPD?
Continue LAMA; corticosteroid and/or LABA combination inhaler; consider other pharmacological interventions.
What are the three broad categories of medical management for COPD patients?
1) inhaled bronchodilators etc.
2) oral theophylline or mucolytics.
3) oxygen
What are the advantages of short acting bronchodilators in COPD? What are examples of such? How long do they take to take effect, and how often can they be given?
The advantage is a rapid onset of action.Short acting beta agonists (SABA) e.g., salbutamol, terbutaline act on bronchial smooth muscle wall to stimulate bronchodilation, reduce gas trapping and the work of breathing. They take 5 minutes to take effect and can be given every 2-4 hours.Short acting muscarinic antagonists antagonise cholinergic nerves in the bronchoconstrictor pathway to allow smooth muscle relaxation. This is effective as the airway resting tone in COPD is often increased. SAMA work in 15 minutes and can be used every 6 hours. Ipratropium bromide is the most widely used.
What are the indications for referral for assessment for oxygen therapy in COPD patients?
1) Central cyanosis.
2) Raised JVP (indicative of right heart failure).
3) Peripheral oedema.
4) FVC1 less than 30%.
5) Sats less than 92% on room air at rest.
6) Polycythaemia.
What is the only long acting muscarinic antagonist? How often is it taken and how long does it last? What effect does it have?
What stage in the GOLD framework is it used?
Tiotropium bromide.
It is taken once a day, works for 36 hours, and slows rate of FEV1 decline, and reduces wheezing, dyspnoea, exacerbation rates, and the amount of rescue medication needed.
It should NOT be taken with its short acting alternative.
It is used in stage 2 GOLD upwards.
What is the role of oral corticosteroids in COPD? Are they used long term?
They have a role in managing exacerbations, but not really in long term maintenance. Despite this 5% of COPD patients are on low dose oral corticosteroids long term.
If needed, keep the dose as low as possible and consider protection from side effects (e.g., bone protection, gastric irritation).
Side effects include osteoporosis, gastritis, adrenal suppression, and hypertension.
What is the mechanism of action of theophylline in COPD? (5)
It is unclear! Thought to act at multiple sites including:
1) relaxing airway smooth muscle.
2) Increasing diaphragmatic strength.
3) Increase mucocilliary clearance.
4) Improve the response to steroid therapy.
5) May also increase cardiac output to further enhance cardiorespiritory function.
When giving theophylline, what should have been tried first?
What side effects might indicate a need to cease therapy (7!).
When should it absolutely not be given?
When starting it, patients should have already been tried on LABA + SABA or LAMA.
Side effects that may indicate a need to discontinue include:
1) Seizures.
2) Diarrhoea.
3) Arrhythmias.
4) Sleeplessness.
5) Allergic reaction.
6) Vomiting,
7) Confusion.
Should absolutely NOT be given if any form of liver dysfunction.
In a patient given theophylline, what measurement is needed and why?
What drugs might interact with theophylline?
What route is it given by?
There is a need to regularly measure plasma levels, as they may reach toxic levels.
It can interact with many thanks that change the metabolism and therefore concentration, but most notably macrocodes and fluroquinolone (which is sometimes given during exacerbations); also smoking messes it up!
There is a slow release oral preparation, but in hospital it tends to be given IV.
What are the long acting beta agonists?
How long do they last?
What GOLD stage should they be introduced in COPD?
Should they be used with SABA’s?
They can be used with their short acting beta-agonist versions (unlike LAMA’s).
Used in GOLD 2 and above.
Examples include formoterol and salmeterol.
They last around 12 hours (while LAMA’s last around 36).
What advantages of LABA’s been shown to have?
They reduce night-time waking, dyspnoea, exercise-induced dyspnoea, and need for rescue agents.
When should inhaled corticosteroids be used in COPD?
GOLD 3 or 4 if symptoms are not adequately controlled by bronchodilators.
Also might be used if there is thought to be a reversible (asthmatic) component to the COPD in the patient in question. This might be the case if they have relatively mild disease by FEV1 criteria, but still have significant clinical symptoms.
What stand alone corticosteroid inhalers are licensed for COPD?
What are the potential side effects of inhaled corticosteroids?
When should the use of inhaled corticosteroids be reviewed?
There are NO stand alone inhaled corticosteroids licensed for COPD!
Preparations are mixtures of corticosteroid and LABA.
Side effects include increased risk of non-fatal pneumonia.
The use of inhaled corticosteroids should be reviewed if they have no effect on the number of exacerbations, lung function, or symptoms.
Is there a role for long term antibiotics in COPD?
If not, why not?
If so, which one(s) and why? And when should they be started?
What sub-group of patients with a co-morbidity might it be of especial use in, and how could they be identified?
Generally, there is no role for long term abx.
It will select out resistant organisms and there is the risk of side effects.
That said, there is research that azithromicin might be of benefit, as it might also have an anti-inflammatory action.
If started, it should be done by secondary care, either after an inpatient admission or an outpatient appointment.
It may be of especial value in patients who also have bronchiectasis (these can be detected by HRCT, also high sputum volume production in the morning suggests bronchiectasis).
What is the role of mucolytics in COPD? What mucolytics are there? Why might it not be a good idea to use one of them?
In theory, they increase the ability to expectorate mucus.
It may have a role in patients with a chronic productive cough, but has no role in preventing exacerbations.
Carbocystine orally is most commonly used.
Nebulised hypertonic saline or water is also used, but this is controversial and perhaps should not be, as it can introduce infection and cause acute bronchospasm.
If there is no clear symptomatic improvement over time, then the mucolytic should be stopped.
Are there other, non-conventional oral therapies for COPD?
1) Antioxidants have been tried, but no clear benefit.
2) Monteleukast is NOT for COPD only asthma.
3) PDE-4 inhibitors show some promise, perhaps by increasing smooth muscle relaxation and by reducing inflammation, but it is not approved for routine use in GP.
How can home oxygen therapy help COPD patients?
1) Symptomatically/improving quality of life - less dyspnoea on execration or rest.
2) Increase long term survival by reducing cardiac strain and improving pulmonary haemodynamics.
When a specialist assessment for HOOF for COPD patients is carried out (i.e., in secondary care by specialists) what will this involve?
Two separate ABG’s at least 3 weeks apart.
HOOF is indicated if Pa02 is less than 7.3 of less than 8 with polycythemaea, pulmonary hypertension, or nocturnal 02 sats less than 90% for more than one third of the night.
What is the most notable side effect of inappropriate HOOF Rx for COPD patients? What must they be advised never to do?
The main adverse affect is respiratory depression. Patients must be warned NEVER to smoke near oxygen cylinders.
How many hours a day should HOOF be used by COPD patients for it to be effective? How is it delivered?
Should be given for at least 15 hours a day.
Can be given via a face mask or nasal cannulas;there may be provision of ambulatory oxygen cylinders so the patient can leave the house.
What if a COPD patient on HOOF becomes significantly hypercapnic or acidotic on oxygen?
They should be assessed for home non-invasive ventilation. This is especially true if they have co-morbidities such as sleep apnoea, or recurrent infections causing type 2 respiratory failure.
What vaccinations should COPD patients be offered?
Annual influenza vaccination.
Pneumococcal vaccination.
Which COPD patients should be offered pulmonary rehabilitation?
1) Patients who consider themselves functionally disabled by COPD.
2) Patients who are GOLD stage 1, 2, or 3
3) A score of 3 or more on the MRC dyspnoea scale.
Who leads pulmonary rehabilitation programs?
What is the benefit?
How long does the benefit last?
Usually respiratory physiotherapists and nurse specialists.
Benefits last for 12 months, and can be repeated if the patient starts to deteriorate.
They improve quality of life and decrease utilisation of healthcare resources.
Why is good nutrition important in COPD?
patients with COPD are often undernourished due to:
1) Difficulties in mastication while dyspnoeic
2) Increased energy demands of laboured breathing.
There is a correlation between being undernourished and having more exacerbations, decreased muscle strength, decreased immunity, and overall mortality.
Try to measure BMI at review and stress importance of energy (especially protein), consider dietician referral.
What is the impact of psychological factors in COPD?
Like anxiety and depression often result.
As a GP you can attempt to manage this with regular anti-depressant/anti-anxiety drugs, and various therapeutic interventions.
This may not be enough, especially for those with dyspnoea in the absence of hypoxia, in which case referral to clinical psychologist or psychiatrist may be helpful. The last resort should be starting something with potentially dangerous side effects - notably opioids and benzodiazepines - due to the risk of respiratory depression and other side effects.
Respiratory physicians and palliative care involvement may also give advice on prescription of these drugs.
Is there a role for palliative care in COPD patients? If so, what things might be discussed?
Yes! As the disease progresses and as GOLD 4 is reached, input from palliative specialisists may be useful. Things that can be discussed might include:
1) Advanced directives.
2) Ceiling of care
3) Ventilators in the end of life setting
4) Potential use of opioids and benzo’s
Patients should be encouraged to have friends/family present as required during these meetings.
Has Hospital at Home (HAH) been shown to reduce admissions in COPD patients?
No, unfortunately they have not been shown to reduce admissions or overall mortality. However…
…they have been shown to dramatically improve the patient’s quality of life.
Are people with COPD entitled to benefits? Where can advice be sought?
Maybe, especially if their illness causes significant disability and they are under 65. See department of work and pensions.
For patients with respiratory disease, there are prognostic indicators which indicate end of life is near. Two or more of these mean death is approaching. There are 7 - name them!
1) Signs and symptoms of right heart failure.
2) Disease assessed to be severe.
3) Grade 4 or 5 MRC dyspnoea scale.
4) For COPD, use of over 6 weeks of systemic corticosteroids over a 6 month period.
5) Recurrent hospital admissions.
6) Fulfil the criteria for long term oxygen therapy.
7) A combination of factors including depression, anorexia, and recurrent infections.
How often should patients with COPD be reviewed in primary care, and by whom?
At least once a year for GOLD 1 or 2.
At least twice a year for GOLD 3 or 4.
Should be carried out by a doctor or a specialist nurse.
When COPD patients are reviewed in primary care, what should be asked/done? (There are 12! 7 would be good…)
1) Docu,net smoking status.
2) Patient experience of symptom control.
3) Review complications, including admissions, and need for either steroid or antibiotic therapy for current or emergency use.
4) Side effects of regularly prescribed meds.
5) Assessment of inhaler technique and ? does this patient need a spacer?
6) Consider referral to another member of the multidisciplinary team.
7) Consider enrolment in pulmonary rehab program.
8) Oxygen sats.
9) FEV1 Vs predicted.
10) FVC
11) BMI
12) MRC dyspnoea scale
What might prompt referral of a COPD patient to secondary care (if they are not already under secondary care!) (6)
1) Haemoptysis.
2) Unclear diagnosis
3) Rapid decline
4) Early onset (under 40)
5) Bronchiectasis considered
6) If patient is a possible candidate for lung transplant of for lung volume reduction surgery (i.e., patient’s who remain breathless despite maximal medical and pulmonary therapy)
What are the stages of the medical Research Council dyspnoea scale?
1) Not troubled by breathlessness, except on strenuous exercise.
2) Short of breath when hurrying or walking up a slight hill.
3) Walks slower than contemporaries on level ground because of breathlessness, or has to stop for breath when walking at own pace.
4) Stops for breath when walks about 100 metres or after a few minutes on level ground.
5) too breathless to leave the house, or breathless when dressing or undressing.
According to GOLD criteria, what is absolutely required to make a diagnosis of COPD?
Although there are of course many clinical features that would suggest a diagnosis of COPD, GOLD say that you can only make the diagnosis after spirometry!
How many people in the UK do NICE think are probably living with undiagnosed COPD?
Two million.
Wow.
When a patient with COPD is admitted to hospital, what is the chance of them being readmitted, and within what time frame?
There is a 33% chance of readmission with the media time to readmission of 38 days.
How do the British Thoracic Society define pulmonary rehabilitation?
“An interdisciplinary program of care for patients with chronic respiratory impairment, that is individually tailored and designed to optimise each patients physical and social autonomy. Programs comprise individualised exercise programs and education.
What is the backbone of pulmonary education, I.e., what is the main thing that it comprises?
Short outpatient-based programmes, usually run by a specialist nurse, that centres on aerobic exercise and on education.
What are the general principles of pulmonary rehabilitation? (5)
1) The goals of rehabilitation are to reduce the symptoms, disability, and handicap, and to improve functional independence in people with lung disease.
2) It is assumed that optimal medical management has been achieved or continues alongside the rehab process.
3) The rehab programme incorporates physical training, disease education, nutritional, psychological, social and behavioural interventions.
4) Rehabilitation is provided by a multidisciplinary team, with involvement of the patient’s family, and attention to individual needs.
5) The outcome of the rehab for individuals (and the way the programme is run itself!) should be continually observed, with the appropriate measure of disability, handicap, and impairment being monitored - I.e., is it working?
In pulmonary rehabilitation, how many sessions a week are recommended?
A minimum of twice a week supervised sessions, with the possibility of a third unsupervised session of prescribed exercises.
In pulmonary rehabilitation, how many sessions should be offered/attended?
Although there may be gains from shorter programs those of 6-12 weeks duration demonstrate the most significant benefit, with attendance at a minimum of 12 supervised sessions.
It is sometimes possible to run the sessions in the patient’s home, but practical considerations must be made, e.g., getting the exercise equipment there, staff availability to travel out to a remote location, etc.
Exercise is the main focus of pulmonary rehabilitation programs; what sort of exercise is advised? And what is the aim?
The aim is to increase capacity and to reduce dyspnoea during exercise.
The form of the exercise is usually a combination of endurance/aerobic training, alongside strength/resistance work, delivered in a way that empowers the patient to continue effective exercise once the supervised sessions have ended.
Although this is a generic form of exercise, it is tailored to the individual - e.g., the intensity of exercise and the targets set should be different from patient to patient.
Endurance training is at the heart of pulmonary rehabilitation - what form does this usually take?
It is most usual to consist of walking and/or cycling for 20-30 minutes.
This is guided by intensity, duration, and frequency. One or two of these variables is usually fixed, and the third increased in an effort to improve function and meet the set target. So for example, the duration might be set at a fixed thirty minutes; the intensity is then gradually increased to meet the target.
How do you measure the intensity of an exercise in pulmonary rehabilitation?
Typical measures include heart rate, treadmill speed, resistance on a exercise bike, etc.
