COPD Flashcards
What is the definition of COPD?
a heterogeneous, progressive lung disease state characterised by chronic respiratory symptoms and airflow obstruction that is not fully reversible
What causes obstruction of airflow in COPD?
- Inflammation of the airways:
“chronic bronchitis” - Destruction of the alveolar wall w/ dilation of the airspace:
“emphysema”
(the inflammation + destruction is triggered by):
1. toxic substances
- tobacco smoke
2. Occupational pollutants
- dust and silica
What is chronic bronchitis?
“Productive cough for > 3 months each year for 2+ consecutive years”
An inflammatory process in which:
- there is an increase in mucus production that obstructs the airway
What is the role of elastases in the body?
the integrity and structure of the resp bronchioles and alveolar wall are dependent on the balance between elastases (which destroy elastin) and anti- elastases (which stop elastase)
What is emphysema?
Destruction & enlargement of the alveoli:
1. An inflammatory response usually triggered by tobacco smoke
2. This tips the balance, increasing the amount of elastases in the body (destroy the elastin in alveolar)
3. Leads to excessive destruction of the alveolar wall
4. Elastic recoil is lost
5. Airways collapse
6. Air is trapped in alveoli
7. Gas exchange is impaired leading to hypoxemia and retention of CO2
(can also be caused by alpha-1 antitrypsin deficiency- usually in people under 45 with COPD)
Describe the mechanism of action by which alpha-1 antitrypsin deficiency leads to emphysema
For people < 45 YO with COPD:
- Alpha- 1 antitrypsin deficiency is an autosomal dominant disorder
- Usually alpha-1 antitrypsin is synthesised in the liver and inhibits neutrophil elastase
- With the disorder, this protein is not exported out of the liver; elastase accumulates
- causes damage to the lung parenchyma and liver cirrhosis
onset of symptoms occurs early in smokers vs non-smokers
What are the risk factors for COPD?
- Smoking - predominantly affects upper lobes (as they are better ventilated)
- Air pollution / Environmental toxins (dust, nitrogen dioxide)
- Cadmium, coal, cotton, cement and grain
- Advanced age
- Genetic factors (alpha-1 antitrypsin deficiency)
- Lung growth + development
Summarise the epidemiology of COPD
● VERY COMMON (8% prevalence)
● Presents in middle age or later
● More common in males - this may change because there has been a rise in female smokers
What are the presenting symptoms of COPD?
- Chronic productive cough
- Breathlessness (initially at exercise - reducing exercise tolerance, eventually at rest)
- Fatigue
- Sputum production
- In severe cases, chronic changes in the vascular beds causing pulmonary hypertension –> right sided heart failure (cor pulmonale) –> peripheral oedema
- Pink puffers and blue bloaters
What is meant by “pink puffers and blue bloater”?
this refers to the different symptoms experienced by COPD pts with bronchitis vs emphysema:
BRONCHITIS: “Blue bloater”
- cyanosis
- peripheral oedema
- obesity
- crackles + wheeze
EMPHYSEMA: “Pink puffer”
- Pink skin
- Pursed- lip breathing
- Accessory breathing muscles
- Barrel chest
- Decreased breath sounds
- Cachectic appearance
What symptoms are associated with COPD exaccerbation?
- Upper airway symptoms (colds and sore throats)
- Increased wheeze
- Chest tightness
- Reduced exercise tolerance
- Fluid retention
- Increased fatigue
- Acute confusion
Increased: - Dyspnoea
- Sputum purulence
- Sputum volume
- Cough
What signs of COPD can be found on physical examination?
- Inspection
o Respiratory distress
o Use of accessory muscles – tripod position
o Pursed lip breathing
o Barrel-shaped over-inflated chest
o Decreased cricosternal distance
o Cyanosis
- Tar staining - Palpation
o Reduced expansion - Percussion
o Hyper-resonant chest
o Loss of liver and cardiac dullness - Auscultation
o Quiet breath sounds
o Prolonged expiration
o Wheeze
o Rhonchi - rattling, continuous and low-pitched breath sounds that sounds a bit like snoring. They are often caused by secretions in larger airways or obstructions
o Sometimes crepitations - Signs of CO2 Retention
o Bounding pulse
o Warm peripheries
o Asterixis - RARE - LATE STAGES: signs of right heart failure (cor pulmonale)
o Right ventricular heave
o Raised JVP
o Ankle oedema
What investigations are used to monitor COPD?
- Pulse oximetry
- Spirometry and Pulmonary Function Tests
- CXR- used to rule out other pathologies:
- May appear NORMAL
- Hyperinflation (> 6 anterior ribs or 10 posterior ribs, flattened diaphragm)
- Reduced peripheral lung markings
- Elongated cardiac silhouette
- Bullae - Bloods :
- FBC
- Increased WCC if infective exacerbation
- increased Hb and haematocrit due to secondary polycythaemia(HAEMATOCRIT >55%)
- ABG - may show hypoxia, normal/raised PCO2 (if acutely unwell) - type 2 respiratory failure
- Inflammatory markers - if evidence of exacerbation - ECG and Echocardiogram- check for cor pulmonale (RBBB & right axis deviation) risk factors for COPD are similar to those for IHD (so co-morbidities common)
- Sputum and Blood Cultures- useful in acute infective exacerbations
- a1antitrypsin levels- useful in young patients (<45) who have never smoked
- reduced DLCO due to emphysema
How is COPD confirmed/ diagnosed?
- Spirometry and Pulmonary Function Tests :
Reduced FEV1/FVC <70% & - After PFTs, give inhaled bronchodilator (COPD is irreversible so the bronchodilator SHOULD NOT change PFTs)
- Repeat PFTs, if FEV1 has not increased by at least 12%-> COPD
- In COPD there is also an increased total lung capacity and residual volume (due to air trapping)
How is COPD managed generally- to achieve stable COPD?
General:
o Stop smoking
o Encourage exercise
o Treat poor nutrition or obesity
o Influenza and pneumococcal vaccination
o Pulmonary rehabilitation/palliative care
o PRN short-acting antimuscarinic (ipratropium) or short acting b2 agonist (salbutamol)
