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Flashcards in Respiratory - COPD Deck (25):

What is COPD?

WHO definition of COPD is:
- preventable and treatable disease with some significant extrapulmonary effects
- airflow limitation that is not fully reversible
- airflow limitation is progressive and associated with an abnormal inflammatory response of the lungs

Patients with COPD have chronic bronchitis and emphysema in varying degrees.


What is emphysema?

Emphysema is enlargement of the airspaces distal to the terminal bronchioles with destructive changes in the alveolar wall.

There are a number of different types of emphysema depending on the pattern of airspace enlargement. In centrolobular emphysema, damage is limited to the central part of the lobule around the respiratory bronchiole. In panacinar emphysema there is distruction and distension of the whole lobule.


What is chronic bronchitis?

This is the second disease that forms COPD. It is defined as a daily cough with sputum production for at least 3 months a year for at least 2 consecutive years.

Notice that emphysema is an anatomical definition, whereas chronic bronchitis is a clinical one.


Is COPD the only disease where poorly reversible airflow limitation occurs?

No. All obstructive diseases can have an element of airflow limitation - e.g. bronchiectasis, CF, TB and some cases of chronic asthma.

Asthma is really the exception because it is characterised by reversible (rather than progressive) airflow obstruction.


What is the pathogenesis of emphysema?

1) Imbalance between protease/ anti-protease system
2) Cigarette smoking results in release of neutrophil elastase (and increased neutrophil margination/ holding up in capillaries)
3) Elastase cleaves elastin AND type IV collagen
4) Type IV collagen in the blood gas barrier may be a particularly critical structure - loss affects gas diffusion


What are the pathological features of chronic bronchitis?

There is mucus gland hypertrophy in chronic bronchitis which extends into the lumen.
Hypertrophic glands secrete large amounts of mucus in response to inhaled pollutants which overwhelms the muco-ciliary escalator.

There are also small airway changes that are likely to be the first changes seen in chronic bronchitis. These include:
- inflammation
- wall oedema
- narrowing
- cellular infiltration
- peribronchial fibrosis


What reduction in FEV1 and FEV1/FVC is required to diagnose airflow obstruction?

On spirometry a reduction in FEV1 to <80% of predicted and an FEV1/FVC of <0.7 suggests airflow obstruction. The key in COPD is that this is poorly reversible.


What are some important aetiologies for COPD?

1) Age - rarely clinically significant in patients less than 50 years of age due to its natural long history

2) Cigarette smoking - most important; severity of clinical disease is related to the number of cigarettes smoked

3) Environmental - morbidity and mortality related to the degree of general atmospheric pollution, but this effect is only significant in smokers

4) Infection - viral and bacterial infections are important in acute exacerbations of COPD; not causative

5) Allergic predisposition - allergic factors may have a minor role in the aetiology of persistent airflow limitation

6) Hereditary factors - alpha 1 antitrypsin is a rare but important predisposition to the development of emphysema

7) Individual susceptibility - not ALL smokers develop COPD


What are the signs and symptoms of COPD?

Symptoms - cough, sputum, dyspnoea, wheeze

Signs - tachypnoea, use of accessory muscles of respiration, hyperinflation, decr. cricosternal distance, decr. expansion, resonant or hyper-resonant percussion note, cyanosis, cor pulmonale, wheeze


What are pink puffers and blue bloaters? Which group are in danger of hypercapnic respiratory failure?

The clinical presentation of COPD is varied as patients have a variable degree of chronic bronchitis and emphysema. Pink puffers and blue bloaters are at the ends of spectrum of presentation.

Pink puffers: have increased alveolar ventilation, a near normal PaO2 and a normal or low PaCO2 (due to hyperventilation). They are breathless but not cyanosed. They may progress to type 1 respiratory failure.

Blue bloaters: have decreased alveolar ventilation, with low PaO2 and high PaCO2. They are cyanosed but are not breathless and may go onto develop cor pulmonale. There respiratory centres are relatively insensitive to carbon dioxide and they rely on hypoxic drive to maintain respiratory effort - give supplementary oxygen with caution.


What are the complications of COPD?

- acute exacerbation +/- infection
- polycythaemia (due to hypoxia)
- respiratory failure
- cor pulonale (oedema, raised JVP, palpable liver)
- pneumothorax (ruptured bullae)
- carcinoma (due to smoke exposure)


Why do patients with COPD have hyperinflated chests?

This correlates with the degree of emphysema. There is loss of elastic recoil from loss of alveolar walls, air trapping and a reflex reaction where the patient breathes at a higher FRC to maintain small airway patency*.

* Lung volume alters airway resistance because of radial traction exerted on the airways by the surrounding lung tissue. High lung volumes are associated with lower resistance because of increased traction on airways. Patients with increased airway resistance due to obstruction "learn" to breathe at higher lung volumes to offset the high airway resistance associated with their disease.


Why do patients with COPD have impaired maximal respiratory airflow?

FEV1 is reduced because of airway obstruction (from distortion, fibrosis and mucus production).

FVC is reduced because of premature airway closure towards the end of expiration. This is caused by dynamic compression of the airways. Loss of elastic recoil from loss of alveolar wall support leads to increased or earlier airways closure for any expiratory pressure.


How is gas exchange affected in COPD?

COPD is associated with V/Q inequality which caused hypoxaemia, CO2 retention, increased A-a difference, increased physiologic dead space, increased physiologic shunt.

Distribution of V/Q inequalities is slightly different for type A (pink puffers) and type B (blue bloaters) patients:
- Type A patient: large amount of ventilation to regions of lung with high V/Q ratios (i.e. large ventilation with low blood flow); capillaries destroyed by emphysematous process --> physiologic dead space; no hypoxia because blood diverted by hypoxic pulmonary vasocontriction

- Type B patient: large blood flow to poorly ventilated regions (low V/Q ratios) leading to cyanosis


What investigations are used to diagnose COPD?

1) CXR: hyperinflation (>6 anterior ribs visible), flat hemidiaphragms, large central pulmonary arteries, decr peripheral vascular markings, bullae

2) FBC: polycythaemia

3) ECG: right atrial and ventricular hypertrophy

4) ABG: hypoxia +/- hypercapnia

5) Lung function: FEV1 <80% predicted, FEV1/FVC <0.7, incr. TLC, RV and decr DLCO

NB - alpha 1 anti-trypsin deficiency tends to affect the lung bases rather than smoking related COPD which affects the whole lung


How should COPD be managed? When should antibiotics be used?

1) Smoking cessation is a priority

2) Bronchodilators: beta agonists or anti-muscarinics are used in the 20-40% of those who benefit. A 2 week trial of oral steroids should be considered to determine reversibility of airway obstruction if a diagnosis of untreated asthma is suspected. Long acting drugs are recommended for all patients who are still symptomatic on short acting therapy and in patients with >2 exacerbations per year. But the next step is determined by the FEV1:
- FEV1 > 50%
i) long-acting beta2-agonist (LABA), for example salmeterol, or:
ii) long-acting muscarinic antagonist (LAMA), for example tiotropium

- FEV1 <50%
LABA + inhaled corticosteroid (ICS) in a combination inhaler, or:

3) LTOT: for >16 hours daily prolongs life in patients with chronic respiratory failure (i.e. those with a PaO2 of <7.3kPa and FEV1 of <1.5L)

4) Antibiotics: used in acute infective exacerbation. Oral steroids improve recovery from acute exacerbations. Long term inhaled steroids reduce the frequency of exacerbations in those with moderate disease and should be used in those with an FEV1 of <50% and at least 1 exacerbation per year

5) Pulmonary rehabilitation

6) Surgery to resect large bullae (enables adjacent areas of lung to reinflate)


When can theophylline be considered in patients with COPD?

NICE only recommend a trial of oral theophylline after trials of short and long acting bronchodilators or for people who cannot used inhaled therapy. The dose should be reduced if macrolide of fluoroquinolone antibiotics (e.g. ciprofloxacin) are co-prescribed.


How should cor pulmonale be treated?

Features include peripheral oedema, raised jugular venous pressure, systolic parasternal heave, loud P2
use a loop diuretic for oedema, consider long-term oxygen therapy
ACE-inhibitors, calcium channel blockers and alpha blockers are not recommended by NICE


What factors improve survival in patients with COPD?

Smoking cessation - the single most important intervention in patients who are still smoking
Long term oxygen therapy in patients who fit criteria
Lung volume reduction surgery in selected patients


What are the adverse side effects of nicotine replacement therapy? What forms can it be given in?

Adverse effects include nausea & vomiting, headaches and flu-like symptoms
NICE recommend offering a combination of nicotine patches and another form of NRT (such as gum, inhalator, lozenge or nasal spray) to people who show a high level of dependence on nicotine or who have found single forms of NRT inadequate in the past. Oral NRT is not available as nicotine has poor absorption from the GIT.


What is varenicline and how long should it be used for smoking cessation?

Varenicline is an alpha receptor partial agonist. It should be started 1 week before the patients stop date (patients who want to quit smoking are encouraged to identify a stop date). The recommended course of treatment is 12 weeks.


What side effects are associated with varenicline?

Nausea is the most common adverse side effect. Other problems include headache, insomnia and abnormal dreams. Varenicline should not be given to patients with a past medical history of depression. It is also contraindicated in pregnancy and breast feeding.


What is buproprion?

This is a noradrenaline and dopamine reuptake inhibitor, and nicotinic antagonist. This should be started 1-2 weeks before the patients stop date. Side effects include a small risk of seizures, and is contraindicated in epilepsy, breast feeding and pregnancy. Eating disorders are a relative contraindication.


What are the NICE guidelines regrading prescribing smoking cessation?

Do not prescribe NRT, varenicline or buproprion in combination.
If all 3 methods fail they should not be represcribed within 6 months.
Prescriptions should only be given to last 2 weeks after the patients stop date. Normally this will be 2 weeks for NRT and 3-4 weeks for verinicline and bupropion. This is to allow for the different methods of administration and mode of action. Further prescriptions should be given only to people who have demonstrated that their quit attempt is continuing.


How is smoking cessation managed during pregnancy?

The first-line interventions in pregnancy should be cognitive behaviour therapy, motivational interviewing or structured self-help and support from NHS Stop Smoking Services.
The evidence for the use of NRT in pregnancy is mixed but it is often used if the above measures failure. There is no evidence that it affects the child's birthweight. Pregnant women should remove the patches before going to bed.
Varenicline and bupropion are contraindicated

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