Session 7 Flashcards
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.
What are the advantages of lung cancer screening?
Detects disease before critical point, causes little morbidity, affordable, available, allows earlier treatment so better prognosis.
What are the disadvantages of lung cancer screening?
Detects some pseudo-disease so can lead to overdiagnosis.
How is lung cancer staged?
Using TNM staging based on primary tumour, lymph nodes and metastases.
Which stages of lung cancer are operable?
IA-IIB.
Which stages of lung cancer are non-operable?
IIIA.
Which stages of lung cancer are palliative?
IIIB and IV.
Where does lung cancer typically spread to?
Brain, draining lymph nodes, pericardium, lungs, pleura, liver, adrenal glands, bone.
How is lung cancer staged?
Using imaging (usually CXR) and tissue sampling.
What are the typical presenting symptoms of lung cancer?
Cough, dyspnoea, wheezing, haemoptysis, lung infection, chest/shoulder pain, weight loss, lethargy/malaise, metastatic symptoms (bone pain, bloated face, hoarseness, etc.), metabolic symotoms (hypercalcaemia, hyponatraemia).
What is paraneoplastic syndrome?
Consequence of cancer in the body where the syndrome isn’t due to the presence of local cancer cells.
What paraneoplastic symotoms can occur in lung cancer?
Hypercalaemia, Cushing’s syndrome, SIADH, anaemia, thrombocytosis, peripheral neuropathy, dermatomyositis, finger clubbing.
Describe the pathology of lung cancer.
Carcinoma (invasive malignant epithelial tumour). Usually non-small cell lung cancer but may also be small-cell or other rare tumours. Molecular markers are EGFR, ALK, KRAS and PD1 mutations.
How is lung cancer treated?
Surgery if operable; radical/palliative radiotherapy; combination chemotherapy if appropriate; combination chemo-radiotherapy; biological therapies; palliative care.
