Chronic obstructive pulmonary disease (COPD) Flashcards
(C)
Define COPD
COPD is a chronic progressive obstructive disease of the airways with the two main components being chronic bronchitis and emphysema.
It is an umbrella term for the those two, and you can have one and not the other or have both.
What are the two components of COPD?
Chronic bronchitis
Emphysema
How does tobacco smoking lead to COPD - aetiology?
Tobacco smoke has many noxious chemicals and ROS. These cause tissue damage inducing an inflammatory response resulting in IL-8 and TNF-a release. These cause macrophage and neutrophil activation and trafficking = release proteases (trypsin, elastase, MMPs) which degrade the structural proteins so more damage and tf more inflammation.
The protease damage is even worse as the initial noxious chemicals and ROS cause antiprotease inactivation.
The tissue damage also causes impaired muco ciliary clearance so increased risk/more resp infections -> more inflammation.
Long term tissue damage -> tissue remodelling + thickening -> obstruction -> decreased respiratory function.
What is chronic bronchitis and describe its pathophysiology
It is long-term inflammation of the bronchi and characterised by chronic and excessive sputum production, coughing and airway obstruction.
Cilia damage + mucus hypersecretion → Impaired mucocilliary clearance → Inc. risk of (Recurrent) Infection
Inflamed and swollen airway tissue/oedema → Irritation of sensory neurones → Cough (also caused by the excess mucus)
Loss of elastin -> weakened airway structure and loss of airway patency (Airway collapses)
long term -> airway remodeling and thickening causing more obstruction
the proteases arent as prominent in this, it has bigger role in emphys
What is emphysema and its pathophysiology (how it develops)?
This is pathological enlargement of the distal airspaces in the alveoli due to alveolar wall degradation (so leading to merging). This can be detected on imaging e.g. CT
Patho = Inflammation in the lungs is usually countered by antiproteases (e.g. alpha-1 antitrypsin). Tobacco smoke’s noxious chemicals/ROS cause inactivation of these antiproteases.
Tf proteolytic enzymes (e.g. elastase) produced by macrophages/neutrophils break down the alveolar walls leading to enlargement of the terminal air spaces, reducing the SA available for gas exchange (particularly elastin). Loss of elastin in emphysema is what causes most of the air trapping.
What are the main causes of COPD?
Tobacco smoking causes 90% of cases (incl passive, in utero). However, only 10% of smokers develop it which means there are other co factors involved (e.g. genetic pre dispositions)
Other causes include:
Alpha-1 Antitrypsin Deficiency (particularly emphysema)
Occupational exposure to dusts and fumes
Household air pollution from wood or coal burning
What risk factors may make prognosis worse for COPD?
Age, ongoing smoking, reduced body weight, severe obstruction on spirometry (measured low FEV1), poor exercise tolerance, cor pulmonale
What are the clinical symptoms of COPD?
Productive cough
Dyspnea (worse in exertion)
Wheeze
Recurrent lower respiratory tract infections
In more advanced cases, systemic symptoms such as weight loss and fatigue may be present
What are the clinical signs of COPD?
Wheeze, coarse crackles, Hyperinflation of lungs (barrel chest), Pursed lip breathing, Accessory muscle usage, Cyanosis
Signs of cor pulmonale in severe COPD:
- Peripheral oedema
- Left parasternal heave
- Raised JVP
- Hepatomegaly
What are the differentials of COPD?
Asthma
Bronchiectasis
Heart failure
Pulmonary fibrosis
Lung cancer
TB
What are the investigations to diagnose COPD?
- Post-bronchodilator spirometry is the diagnostic test and is key to classifying severity. A post-bronchodilator FEV1/FVC ratio <0.7 confirms obstruction.
- CXR = may show symptoms of hyperinflation, bullae, flat hemidiaphragm. Also important to exclude lung cancer/bronchiectasis
- Bloods = FBC to see if secondary polycythaemia (copd can cause) or anaemic (exacer factor),
- Bloods = Alpha-1 antitrypsin levels in young pts/little smoking
- Body mass index (BMI) calculation
CT scan if suspecting alternative diagnoses (fibrosis, cancer or bronchiectasis)
Who does NICE recommend investigating for COPD?
NICE recommend considering a COPD diagnosis in pts over 35 years who are smokers or ex-smokers and have symptoms such as exertional breathlessness, chronic cough or regular sputum production.
What confirms diagnosis of COPD?
a post-bronchodilator FEV1/FVC ratio of <0.7
What investigations may be done if cor pulmonale is suspected in COPD?
- BNP levels in blood
- Echo
How is COPD severity classified?
The severity can be graded using the forced expiratory volume in 1 second (FEV1):
Stage 1 (mild): FEV1 more than 80% of predicted (these pts require symptoms in order to be diagnosed)
Stage 2 (moderate): FEV1 50-79% of predicted
Stage 3 (severe): FEV1 30-49% of predicted
Stage 4 (very severe): FEV1 less than 30% of predicted
Brief outline of COPD management?
All patients with COPD should be offered education, smoking cessation, vaccinations, pulmonary rehabilitation (if indicated) and pharmacotherapy (e.g. inhalers).
What is the non-medical management of copd?
- Patient education, ensure all patients have a personalised self-management plan
- Smoking cessation support
- Nutritional support
- Annual Flu and one off pneumococcal vaccinations
- Pulmonary rehabilitation if indicated
Where is pulmonary rehabilitation indicated + contraindication in COPD?
Ind: offered to any patient with COPD who view themselves as functionally disabled by their condition (usually MRC grade 3 and above)
Contraind: patients unable to walk, unstable angina or have had recent MI
What is pulmonary rehabilitation?
PR is an exercise and education program for people with chronic lung disease tf COPD. It involves:
- Exercise training
- Breathing techniques
- Education
When is pharm management offered to COPD pts?
Inhaler therapies are offered if needed to relieve shortness of breath that limits their activities e.g. exercise limitation
What is first line management of COPD and examples?
Offer a SABA (e.g. Salbutamol) or SAMA (e.g. Ipratropium) for patients to use on as needed basis
What is the second step of management if symptoms still persist in COPD or have acute exacerbations? give one example of each med
Offer LABA+LAMA if no evidence of steroid responsiveness or asthmatic features)
OR
Offer LABA+ICS if evidence of steroid responsiveness or asthmatic features
LABA = Salmeterol, LAMA = tiotropium, ICS = beclomethasone
What is the third step of management if symptoms still persist in COPD or have acute exacerbations? when is it specifically indicated
Offer escalation to triple therapy - (LABA + LAMA + ICS)
Indicated if:
Clin features affect QoL then offer 3 month trial. If no improvement, revert back to LABA + LAMA only
Or
1 severe or 2 moderate acute exacerbations within one year
Give example of LABA and ICS combination inhaler
Seretide (salmeterol/fluticasone)
Give example of LABA and LAMA combination inhaler
Ultibro (indacaterol/glycopyrronium)
Give example of a triple therapy combination inhaler for COPD
Trimbow (formoterol/glycopyrronium/beclometasone)
Give examples of LABAs
Salmeterol, formoterol and indacaterol
Give examples of LAMAs
tiotropium, glycopyronium
Give an example of an inhaled corticosteroid (ICS)
Beclomethasone
How are COPD patients assessed for long term oxygen therapy?
- Must have stable COPD (not recovering from recent exacerb)
Patients then have two ABGs in air at least 3 weeks apart to see if they meet the criteria.
When is there indication for long term oxygen therapy in COPD (criteria) and how long is it used?
LTOT is reserved for patients with stable COPD and meet this criteria:
Arterial Pa02 < 7.3 kPa
OR
Arterial Pa02 < 8 kPa with any of:
Pulmonary hypertension
Peripheral oedema
Secondary polycythaemia
Required for at least 15 hours a day to see benefit. No smoking while using it bc risk of fire/burn.
When is there indication for surgery in COPD, give example of surgery
Rarely, surgical intervention may be offered to some patients. Recommended NICE one is lung volume reduction surgery (removing emphysema areas so that the healthy lung can expand)
E.g. pts with severe COPD who remain breathless despite maximal medical therapy
What are complications of COPD?
- Acute exacerbation
- Cor pulmonale
- Recurrent pneumonia
- Pneumothorax
- Respiratory Failure (T2)
- Secondary polycythemia
What is emergency presentation of COPD?
An acute exacerbation of COPD.
This is sudden worsening in airway function and respiratory symptoms in patients with COPD
Pts often require admission to hospital for treatment.
Worsening breathlessness
Worsening cough
Increased sputum production/Change in colour
Wheeze
Common causes of COPD acute exacerbations?
Bacterial or viral resp infections (most common = rhinovirus)
Smoking
Env pollutants
Most exacerb are not bacterial.
What is emergency management of COPD severe acute exacerbation?
Bronchodilators: usually given as nebulisers (SABA or SAMA e.g. Salbutamol or ipratropium)
Oxygen therapy using venturi mask if needed: Do not over oxygenate (keep 88-92%) bc COPD pts at risk of hypercapnia (too much O2 -> reduced hypoxic drive -> hypovent -> worse hypercapnia)
Corticosteroid = Prednisolone 30 mg once daily should be given for 5 days
Only give ABs if sputum is purulent or there are clinical signs of pneumonia (1st line are amoxicillin, Clarithromycin, Doxycycline
