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Flashcards in COPD Deck (14):

Explain COPD to a patient

Chronic obstructive pulmonary disease is a degenerative chronic respiratory condition. COPD is not reversible and is progressive, but progresses slowly over several months/years. COPD causes airway obstruction due to narrowing and damage to the areas of gas exchange.

COPD is caused by smoking and therefore the best treatment to slow progression is to stop smoking, completely.

COPD causes a shortness of breath, a long-term cough with sputum production. COPD patients often havemore frequent chest infections. If you have cold/chest infection symptoms you will need to come to the GP immediately as it can progress faster than in a healthy person.

The progression of COPD depends entirely on things you can do e.g. stopping smoking, but also using inhalers and medication when needed and seeking help early.

There are several inhalers we can try, similar to inhalers that asthmatics use. We can also give you oxygen if needed, but we will need to be cautious about how much oxygen we can give because COPD patients should only receive a limited amount. Therefore it is important to always tell medical professionals that you have COPD before they give you oxygen.


What are the 3 symptoms of COPD?

Chronic cough
Sputum production

[Winter exacerbation, wheeze]


What causes COPD?

Genetic susceptibility - alpha-1 anti-trypsin deficiency (increases the sensitivity of the lungs to tobacco smoke and therefore can develop COPD much younger)
Mineral dusts (coal)
Biomass Fuel


What effects can tobacco have throughout the body?

MSK: weakness, cachexia
Bone: osteoporosis, osteopenia
Metabolic: Diabetes, obesity
CVS: IHD, cardiac failure, hypertension
RS: Lung cancer, COPD


What is the pathogenesis of COPD?

Epithelial cells are normally a barrier to exogenous products, but they allow the passage of tobacco toxins to pass to antigen presenting cells, and this activates the immune system (T lymphocytes, proteases, and fibroblasts)

Goblet cell hyperplasia = cough + sputum
Airway narrowing = Dyspnoea + wheeze
Alveolar destruction = Breathlessness


How does COPD present on a respiratory examination?

Use of accessory muscle
Barrel shaped chest
Pursed lips
Increased respiratory rate
[on low volume oxygen]
Tar stained fingers
Central cyanosis
Paradoxical lower chest motions
Reduced breath sounds
Palpable liver edge


How do we investigate for COPD and what do the investigations show?

- FEV1 / FVC ratio = <0.7 / 70%
- Obstructive airway disease
- FEV1 is significantly lower than normal and then graph gradually increases to a slightly lowered FVC
- Increased residual volume
- Increased total lung capacity

- Hyper-inflated lungs
- Flattened hemi-diaphragm

CT scan
- Alveolar destruction (emphysema - small pockets)
- Bronchial wall thickening


Draw a Spirometry curve and flow-volume loop for normal respiration, obstructive and restrictive pictures

*See notes


How does expiration in COPD compare to normal expiration? (Diagrams)

Normal expiration
The expiratory muscle contract and create a positive pleural pressure (+4) and this is transmitted to the rest of the lungs. If there is a resting pressure of +2 in the alveolar this will create a total pressure of +6. This creates a pressure gradient along the airway such that air will flow out of the body.
There are points in the airway here the resting pressure is less than +4, but because the airway is healthy, the structural integrity is maintained and air is expelled.

COPD expiration
In COPD the airway integrity isn't maintained. This is due to airway damage and alveoli damage. In COPD, when a respiratory manoeuvre is performed, the airway will develop a 'pinched point' where the pressure outside the airway is +4 and the pressure inside is +3. This causes the airway to narrow and therefore reduce airflow. This causes the alveoli to distend and so gas is trapped in the chest. This increases the residual volume and total lung capacity.


How is COPD staged?

Global strategy for obstructive lung disease (GOLD)

Stage I FEV1 is >80% predicted
Stage II FEV1 is 50-79% predicted
Stage III FEV1 is 30-49% predicted
Stage IV FEV1 is <30% predicted


What is 'Cor pulmonale' and how does it arise?

The hypoxia present in COPD causes pulmonary arterial vasoconstriction. This is a natural defense mechanism to shunt blood away from hypoxic areas towards non-hypoxic areas. This is useful in localised condition (e.g. pneumonia) but not in generalized conditions (e.g. COPD) when the lung is generally hypoxic. This mechanism causes an increase in pulmonary artery pressure which causes RIGHT VENTRICULAR HYPERTROPHY and eventually RIGHT VENTRICULAR FAILURE.

Increased pulmonary pressure, right ventricular hypertrophy and right ventricular failure all cause 'cor pulmonale'. Cor Pulmonale = right ventricular failure secondary to chronic lung disease

Once right ventricular failure occurs the prognosis for these patients decreases and its often this that causes death.


How is COPD treated?

1. Stop smoking
2. Inhaled bronchodilators
3. Inhaled corticosteroids
- Beclometasone
4, Oral theophylline
5. Aminophylline
6. Mucolytics

Oxygen (short bursts for symptom relief)
Pulmonary rehabilitation
End of life care


How do COPD exacerbations present?

COPD exacerbation's are usually pneumonia

- Preceeding coryzal symptoms
- Increased dyspnoea
- Increased cough
- Increased sputum production
- Increased wheeze
- Increased ankle oedema

- Sputum culture


How do you treat/manage a COPD exacerbation?

Nebulised SABA
Corticosteroids (Oral initially)
Antibiotics if needed

SABA / SAMA (as required)

If FEV1 is >50% = LAMA / LABA
If not improved then add ICS = LAMA + LABA + ICS

If FEV1 is <50% = LABA + ICS / LAMA
If not improved then progress to LAMA + LABA + ICS