Session 7 Flashcards
(37 cards)
Define COPD.
Disease characterised by airflow obstruction which is usually progressive, not fully reversible and does not change markedly over several months. it encompasses emphysema and/or chronic bronchitis.
What is the most common cause of COPD?
Smoking.
What is emphysema?
pathological process where there is destruction of the terminal bronchioles and distal airspaces causing loss of alveolar surface area and impairment of gas exchange.
Why do the lungs hyperinflate in emphysema?
The loss of elastic tissue means that the lungs cant resist the natural tendency of the rib cage to expand outwards so hyperinflation occurs.
What is chronic bronchitis?
Chronic inflammation with excess mucus secretion in the large airways of the lungs.
What can cause COPD?
Smoking, alpha-1 antitrypsin deficiency, occupational exposure, pollution.
How does COPD usually present?
Cough and sputum production are usually the first signs, most patients wont present until they become breathless.
What is exacerbation of COPD?
Increased breathlessness, increased cough and increased sputum production compared to the baseline.
What is the MRC dyspnoea score?
A way of quantifying the level of breathlessness in a patient typically used in COPD.
What are typical signs on examination of COPD?
Pursed lip breathing, tachypnoea, using accessory muscles to breathe, barrel chest, wheeze, quiet breath sounds, cyanosis, oedema.
How is airflow obstruction measured in COPD?
Using spirometry.
What does spirometry show in COPD sufferers?
Reduced total expiratory volume as obstructive condition, FEV1.0 us usually low, FEV1.0/FVC is usually low.
How is COPD diagnosed?
Using a combination of the suggestive symptoms and presence of airflow obstruction on spirometry. CXR used to exclude other diagnoses
How is COPD managed?
Stop smoking, bronchodilators, antimuscarinics, steroids, mucolytics, diet supplements, may need oxygen therapy and lung volume reduction.
How do beta-2 agonists work?
Binds to beta-2 receptor activating adenyl cyclase; [cAMP] increases and PKA activated; MLCK is phosphorylated and activated; smooth muscle relaxes and causes bronchodilation in the lungs.
What are the adverse effects of beta-2 agonists used in COPD therapy?
Tachycardia and tremor due to activation of other beta-2 receptors; anxiety; palpatations; hypokalaemia due to increased skeletal muscle potassium uptake.
How do methylxanthines work?
Inhibit phosphodiesterases so less cAMP is broken down, causing bronchodilation.
What are the potential side effects of long term steroid use?
Think skin, bruising, cataracts, adrenal insufficiency, osteoporosis, DM, fluid retention, mental disturbance, GI symptoms, proximal myopathy.
Why is pulmonary rehabilitation performed in COPD?
To prevent deconditioning from social anxiety and inactivity.
When is long-term oxygen therapy offered to COPD patients?
If pO2 is consistently below 7.3kPa (8kPa with cor pulmonale) if patients are non-smokers and don’t retain high CO2 levels.
What is the aim of COPD treatment?
To improve sufferers’ quality of life as the condition can’t be reversed or cured.
How are acute exacerbations of COPD treated?
Controlled oxygen therapy, nebs, steroids, antibiotics if infective, repeat ABG, consider IV bronchodilators.
What are the contraindications to non-invasive ventilation?
Untreated pneumothorax, impaired consciousness, increased upper airway secretions, facial injury, vomiting, agitation, life threatening hypoxia.
Briefly describe the epidemiology of lung cancer.
Most common cancerous cause of death in UK, very low 5 year survival rate, lowest one year survival rate, more common in less affluent socio-economic groups, large link to smoking, link to occupational carcinogens.
