Respiratory Therapeutics - COPD Flashcards
What is COPD
COPD is characterised by airflow obstruction that is not fully reversible. The airflow obstruction is usually progressive in the long term. COPD is predominantly caused by smoking. Other factors, particularly occupational exposures, may also contribute to the development of COPD. Exacerbations often occur which are a rapid and sustained worsening of symptoms beyond normal day‐to‐day variations. COPD produces symptoms, disability and impaired quality of life which may respond to pharmacological and other therapies that have limited or no impact on the airflow obstruction. COPD is the preferred term for conditions in patients with airflow obstruction who were previously diagnosed as having chronic bronchitis or emphysema
Main risk factors for COPD
- Tobacco smoking
- Indoor air pollution (such as biomass fuel used for cooking and heating)
- Outdoor air pollution
- Occupational dusts and chemicals (vapours, irritants, and fumes)
Aetiology
COPD is caused by long term exposure to toxic particles and gases. Cigarette smoking accounts for over 90% of cases in developed countries. In developing countries, inhalation of smoke from biomass fuels used in heating and cooking in poorly ventilated areas are also implicated. In addition, pollution and climate can be implicated. There is some individual susceptibility to developing COPD. Patients who have Alpha1 Antitrypsin deficiency may develop COPD.
Pathophysiology
An increase in numbers of mucus‐secreting goblet cells of the bronchial mucosa occur with COPD. Microscopically, there is infiltration of the walls of the bronchi and bronchioles with acute and chronic inflammatory cells. Lymphoid follicles may develop in severe disease. The epithelial layer may become ulcerated and with time, squamous epithelium replaces the columnar cells. Inflammation is followed by scarring and thickening of the walls which narrows the small airways. The small airways are particularly affected in the disease and initially this may be in the absence of any significant breathlessness.
Squamous cell metaplasia and fibrosis of bronchial walls develops with further progression of the disease.
Symptoms can include:
Symptoms can include:
Chronic cough productive / non-productive
Smoker’s cough
Wheeze (not always present)
Breathlessness
Infective exacerbations with purulent sputum
Cardiovascular function can be affected
Other systems can be affected e.g. hypertension, osteoporosis and metabolic problems can occur
Symptoms can be worsened by:
- Cold
- Foggy weather
- Atmospheric pollution
- In advanced disease – even mild exercise
Signs In severe disease:
Tachypnoea
Prolonged expiration
Intercostal indrawing on inspiration
Pursing of lips on expiration
Poor chest expansion
Hyperinflated lungs
Loss of normal cardiac and hepatic dullness
Carbon dioxide – responsive / insensitive
Heart failure and oedema – rare features and in terminal cases.
Signs in mild cases
in mild cases there may be no signs or a quiet wheeze throughout the chest
Diagnosis
This is based on several factors. There is no single diagnostic test for COPD. A clinical judgement is made on the basis of a combination of history, physical examination and spirometry to confirm airflow obstruction. Examples include the following:
Age > 35 years who have a risk factor (generally smoking) and who present with one or more symptoms
Exertional breathlessness
Chronic cough
Regular sputum production
Frequent winter `bronchitis’
Wheeze
Ask about other factors (see NICE guidance)
Further investigations that should be carried out include:
Post-bronchodilator spirometry Chest X-ray FBC Calculate the patient’s BMI Other additional investigations (see NICE guidance)
The Medical Research Council Dyspnoea Scale is used which grades breathlessness according to level of exertion. There are five grades, 1 – 5, 5 being the most breathless.
Spirometry
Airflow obstruction should be measured at the time of diagnosis of COPD or, if reconsidering diagnosis. Post-bronchodilator spirometry should be carried out to confirm the diagnosis of COPD.
Parameters measured when spirometry is carried out include:
FEV1
FVC
FEV1/FVC ratio
Severity of airflow obstruction can be graded according to the reduction in patient’s FEV1 (see table in NICE guidance).
Types of respiratory failure
There are two main types of respiratory failure which can be classified as follows:
Type 1 – low PaO2, normal or low PaCO2
Type 2 – low PaO2, high PaCO2
Persistence of chronic alveolar hypoxia and hypercapnia leads to constriction of pulmonary arterioles and subsequent pulmonary arterial hypertension. Cardiac output can be normal or increased but salt and fluid retention occur as a result of renal hypoxia.
Patients with advanced COPD may develop ..
Patients with advanced COPD may develop Cor pulmonale
COPD drug therapy all
Beta 2 agonists inhaled
Antimuscarinics
Xanthines
PDE 4 Inhibitors
COPD drug therapy - Antimuscarinics
Antimuscarinics
Short acting - ipratropium
Long acting – tiotropium, aclidinium bromide (NICE ESNM 8), glycopyrronium bromide (NICE ESNM 9)
Combined inhalers
note: Ultibro Breezhaler® 85/43 micrograms (Indacaterol/glycopyrronium) was the first long-acting beta2 agonist (LABA)/long-acting muscarinic antagonist (LAMA) combination inhaler to be approved for chronic obstructive pulmonary disease (COPD). It was launched in December 2014 (see NICE ESNM 33). Please note further products: Anoro/Ellipta® (Umeclidinium/vilanterol) received a European marketing authorisation in June 2014, which is now licensed in the UK as a maintenance treatment to relieve symptoms in adults with COPD (see NICE ESNM 49); Duaklir Genair® (aclidinium/formoterol) received a European marketing authorisation for maintenance bronchodilator treatment to relieve symptoms in adults with COPD in December 2014 (ESNM 57). Spiolto Respimat® 2.5micrograms olodaterol /dose and 2.5micrograms of Tiotropium /dose solution for inhalation cartridge with device (Boehringer Ingelheim Ltd) approved in 2015
COPD drug therapy - Xanthines
Xanthines
Aminophylline, theophylline
Theophylline is not generally effective in exacerbations of COPD. Theophylline is metabolised by the liver. Theophylline can be given orally. Aminophylline can be given orally or by intravenous infusion. They have a narrow therapeutic index.
Plasma-theophylline concentration is measured 5 days after starting oral treatment and at least 3 days after any dose adjustment. A blood sample should usually be taken 4–6 hours after an oral dose of a modified-release preparation (sampling times may vary—consult local guidelines).
Patients receiving aminophylline or theophylline therapy should have their theophylline plasma concentration measured. A plasma-theophylline concentration of 10 – 20mg/litre (55 – 110 micromol/litre) is required for satisfactory bronchodilation (a lower plasma concentration may be effective). Theophylline plasma concentration is increased in patients with heart failure, hepatic impairment, viral infections, in the elderly and by drugs that inhibit its metabolism. Plasma concentration is decreased in smokers, by alcohol consumption and by drugs that induce its metabolism. Aminophylline and theophylline can interact with many medications. It is imperative that pharmacokinetic calculations are performed to avoid sub-therapeutic levels or toxic effects.
