COPD PART 2 Flashcards
General management for COPD
- Smoking cessation: offer nicotine replacement, varenicline or bupropion
- Pulmonary rehabilitation: for patients who are self-perceived as functionally disabled by COPD (e.g. MRC grade ≥3)
- Vaccinations: one-offpneumococcaland annualinfluenza
- Good diet and exercise: esp if obese
Key pharmacological management for COPD
- SABA:short-acting beta2-agonist (e.g. salbutamol)
- SAMA: short-acting muscarinic antagonist (ipratropium)
- LABA: long-acting beta-agonist (e.g. salmeterol)
- LAMA: long-acting muscarinic antagonist (e.g. tiotropium)
- ICS: inhaled corticosteroid (e.g. beclometasone)
- Combination inhaler (Some or all LABA/LAMA ICS)
- Mucolytics (carbocisteine_
- Systemic corticosteroids (prednisolone)
- Azithromyocin
Initial Management according to NICE for COPD
SABA/SAMA - inhaler
Management if symptoms persist according to NICE
If there are no features of asthma: LABA + LAMA - long acting bronchodilators - improve lung function, dyspnoea, exacerbations
If there are features of asthma: LABA + ICS
- If symptoms still persist: LABA + LAMA + ICS
Additional therapies
Nebulisers
Theophylline
Surgery
Oral mucolytic therapy
Phosphodiesterase -4 inhibitors
Complications of COPD
- Pulmonary Hypertension
- Cor pulmonale
- Pneumothorax
- Respiratory failure
- Exacerbation
- Secondry polycythaemia
What is COPD emphysema?
alveolar air sacs become damaged or destroyed.
alveoli permanently enlarge and lose elasticity, and as a result, individuals typically have difficulty with exhaling, which depends heavily on the ability of lungs to recoil.
RFs for COPD emphysema
Smoking
Emphysema usually co -exists whith chronic bronchitis
What happens in normal airflow?
oxygen flows out of the alveoli and into the blood while carbon dioxide makes the reverse commute.
- Normally, there is a low pressure environment in the airways
- elastin in the walls prevents the lungs from collapsing inwards in a low pressure environment
- allows air to be exhaled out
What happens when lung tissue is exposed to irritants (smoke)
Triggers inflammatory reaction
Inflammatory reactions attract various immune cells which release inflammatory chemicals as well as proteases e.g. elastases and collagenases.
What happens in emphysema?
elastin is lost which causes collapse.
This results in:
- Air-trapping distal to the point of collapse
- The lungs becoming more compliant - when air is inhaled, the lungs easily expand and hold onto that air.
- Breakdown of the thin alveolar walls - septa. This reduces the surface area for gas exchange.
Over time what happens in emphysema
Over time, as more and more lung tissue is affected, emphysema can lead to hypoxemia.
This leads to hypoxic vasoconstriction to navigate blood flow away from damaged lung tissue.
Types of emphysema
- Centriacinar
- Panacinar
- Paraseptal
- Irregular
Centriacinar empyhsema
most common pattern. Only damages the central or proximal alveoli of the acinus. It also typically affects the upper lobes of the lungs. This is usually due to smoking.
Panacinar emphysema
- entire acinus is uniformly affected and typically affects the lower lobes of the lungs.
- Often associated with alpha-1 antitrypsin deficiency.
- Alpha-1 antitrypsin is a protease inhibitor and protects collagen and elastin. Without it, the proteases are able to break down the alveolar walls
Paraseptal emphysema
distal alveoli of the acinus are most affected. Typically affects the lung tissue on the periphery of the lobules.
Irregular emphysema
scarring and damage that affects the lung parenchyma
patchily, independent of acinar structure
COPD lab results
- FVC (max air exhaled in one breath): lowered
- FEV1 (first second of air breathed out in a single breath): lowered, more than the FVC
- FEV1:FVC ratio: lowered
- TLC (total lung capacity): increased due to air trapping
Signs of emphysema
- Breathing with pursed lips
- Barrel shaped chest
- Downward displacement of liver
- Cardiac dullness
Symptoms of emphysema
- Dyspnoea
- Cough: could be productive
- Weight loss: due to energy expenditure while breathing
- Signs of CO2retention
- Drowsy
- Asterixis
- Confusion
Management for emphysema
- Smoking cessation
- Supplemental oxygen
- Bronchodilators
- Inhaled steroids
- Antibiotics: for secondary infections
Complications of emphysema
- Pneumothorax: the distal enlarged alveoli in paraseptal emphysema can rupture and cause a pneumothorax.
- Cor pulmonale and right-sided heart failure: extensive vasoconstriction causes pulmonary hypertension and puts pressure on right ventricle
Differential Diagnosis for COPD
▶ Heart failure
▶ Pulmonary embolus
▶ Pneumonia
▶ Lung cancer
▶ Asthma
▶ Bronchiectasis
▶MI
▶ Pneumothorax
▶ Cardiac arrythmia
What has the greatest capacity to influence COPD?
Smoking cessation - healthcare providers should tell people to quit
Pharmacotherapy and nicotine replacement help with long term smoking abstinence rates
Need regular activity and remain active
What have none of the existing medications for COPD done?
Shown conclusively to modify long term decline in lung function
When should you add ICS to long acting bronchodilators (Strongly favours)
Strongly favours use - History of hospitalisations for exacerbations of COPD, 2 or more moderate exacer of COPD per year, blood eosinophils more than 300cells/uL
History of or concomitant asthma
What factors favor use of ICS in long acting bronchodilators? (Mildly favors)
1 moderate exacerbation of COPD per year
Blood eosinophils 100 to < 300 cell /uL
Against use of ICS with long-acting bronchodilators
Repeated pneumonia events
Blood eosinophils < 100cells/ uL
History of mycobacterial infection
Management of COPD exacerbation
Bronchodilators
▶ Salbutamol (SABA)
▶ +/- Ipratropium (SAMA)
▶ Systemic corticosteroids
▶ Antibiotics if signs of infection
When should you use non-invasive ventilation?
▶ Respiratory acidosis
▶ Hypercapnia
▶ Hypoxaemia despite oxygen
Improves respiratory acidosis, decreases respiratory rate, severity of dyspnoea, complications and length of hospital stay.
Decreases mortality and needs for intubation
What is emphysema?
involves loss of alveolar integrity due to an imbalance between proteases and protease inhibitors (e.g. alpha-1 antitrypsin) triggered by chronic inflammation, such as smoking, which causes elastin breakdown
